E. Medical Complications
Robert Teasell MD FRCPC, Manuel Murie-Fernandez MD, Andrew McClure, Norine Foley
E1.
E2.
E3.
E4.
E5.
E6.
E7.
E8.
E9.
E10.
Dysphagia............................................................................................................................ 2
Dysphagia Case Study…………………………………………………………………………..14
Dysphagia Case Study…………………………………………………………………………..24
Dysphagia in a Nursing Home Stroke Patient………………………………………………... 31
Nutritional Issues Following Stroke……………………………………………………………. 35
Deep Venous Thromboembolism……………………………………………………………… 42
Venous Thromboembolism Case Study………………………………………………………. 57
Post-Stroke Seizure Disorders........................................................................................... 62
Central Pain State……………………………………………………………………………….. 73
Urinary Incontinence…………………………………………………………………………….. 81
110 Pages
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E1. Dysphagia
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E1. Dysphagia
E1.1 Introduction to Dysphagia Post Stroke
Q1. Define dysphagia.
Answer
1. Dysphagia is defined as difficulty with swallowing
Q2. Why is dysphagia important following a stroke?
Answer
1. Dysphagia is common following a stroke.
2. Incident rates are high following an acute stroke
3. Associated with increased mortality and morbidity such as malnutrition, dehydration and
pneumonia.
4. Diagnosing and treating dysphagia in stroke patient improves outcomes such as reduced
risk of pneumonia, length of hospital stay and overall health expenditures.
5. Aspiration, the most important clinical consequence of dysphagia, has long been associated
with an increased risk of pneumonia, death and sepsis.
Discussion
Dysphagia is defined as difficulty with swallowing and is a common complication of stroke. The
incidence rates are reported to be between 29-65% in acute stroke patients. Some of the
variability is related to differences in the timing and method of swallowing assessment. The
presence of dysphagia can be identified on the basis of clinical or radiographic examinations, or
both.
The Heart and Stroke Foundation (2002) noted “the presence of dysphagia in stroke survivors
has been associated with increased mortality and morbidities such as malnutrition, dehydration
and pulmonary compromise” (Smithard et al. 1996, Barer 1989, Kidd et al. 1995, Finestone et
al. 1995, Teasell et al. 1994, Gordon et al. 1987, Schmidt et al. 1994, Sharma et al. 2001).
However, emerging evidence indicates that detecting and managing dysphagia in acute stroke
survivors improves outcomes such as reduced risk of pneumonia, length of hospital stay and
overall healthcare expenditures (Smithard et al. 1996).
Aspiration following stroke, the most clinically significant symptom of dysphagia, has long been
associated with pneumonia, sepsis and death. Silver et al. (1984) and Bounds et al. (1981)
reported that pneumonia was the second most common cause of death during the acute phase
of a stroke, with up to 20% of individuals with stroke-related dysphagia dying during the first
year post stroke from aspiration pneumonia (Schmidt et al. 1988). Steele (2002) found that the
number of swallowing difficulties seen in stroke survivors was associated with the length of
hospitalization. Detection of aspiration, both silent and audible, and subsequent adaptive
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management strategies are regarded as important in the prevention of pneumonia (Horner and
Massey 1988a, Horner et al. 1988b, Logemann 1983, Teasell et al. 1996, Tobin 1986, Veis and
Logemann 1985). Management of dysphagia largely focuses on strategies to avoid aspiration
following stroke.
E1.2 The Normal Swallowing Process
Q3. Describe the normal swallowing process.
Answers
Normal swallowing consists of 4 phases:
1. Oral preparatory phase
2. Oral propulsive phase
3. Pharyngeal phase
4. Esophageal phase
Discussion
Normal Swallowing
Normal swallowing has four sequential coordinated phases: the oral preparatory phase, the oral
propulsive phase, the pharyngeal phase and the esophageal phase. Each of the phases of a
normal swallow is described below.
1. Oral Preparatory Phase. During this phase, food in the oral cavity is manipulated and
masticated in preparation for swallowing. The back of the tongue controls the position of the
food, preventing it from falling into the pharynx (Platt 2001).
2. Oral Propulsive Phase. During the oral propulsive, the tongue transfers the bolus of food
to the pharynx, triggering the pharyngeal swallow (Platt 2001).
3. Pharyngeal Phase. During the pharyngeal phase, complex and coordinated movements of
the tongue and pharyngeal structures propel the bolus into the esophagus, while protecting
the airway (Platt 2001).
4. Esophageal Phase. During the esophageal phase of swallowing coordinated contractions
of the esophageal muscle move the bolus through the esophagus towards the stomach
(Platt 2001).
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Oral Preparatory Phase
Food in the oral cavity is
manipulated and masticated in
preparation for swallowing. The
back of the tongue controls the
position of the food, preventing it
from falling back into the pharynx.
1.
Oral Propulsive Phase
The tongue transfers the bolus of
food to the pharynx which triggers
the pharyngeal swallow.
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2. Pharyngeal Phase
Complex and coordinated movements of the tongue and pharyngeal structures propel the
food bolus into the esophagus while protecting the airway.
3. Esophageal Phase
Coordinated contractions of the
esophagus muscle move the bolus
through the esophagus toward the
stomach.
E1.3 Defining Dysphagia and Aspiration
Q4. What is the difference between Dysphagia and Aspiration?
Answers
1. Dysphagia is defined as difficulty with swallowing.
2. Aspiration is defined as entry of oral or gastric material into the airway below the level of the
true vocal cords.
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Discussion
Dysphagia
Dysphagia post stroke is characterized by a delay and reduced function in the pharyngeal
phase of swallowing. Although the incidence of dysphagia is more common following brainstem
or bilateral hemispheric stroke, it frequently occurs following unilateral hemispheric strokes.
Signs and Symptoms of dysphagia include: Choking on food, coughing during meals, drooling
or loss of food from mouth, pocketing on food in cheeks, slow, effortful eating, difficulty
swallowing pills, avoiding food or fluids, complaining of food sticking in throat, problems
swallowing, reflux or heartburn (Schmidt et al. 1994).
Aspiration
Aspiration is defined as "entry of material into the airway below the level of the true vocal cords".
Since many stroke patients with dysphagia do not aspirate, the two terms are not synonymous,
although they are closely associated. The diagnosis of aspiration should be suspected when
the stroke patient has any of the following: a subjective complaint of trouble swallowing, an
abnormal chest x-ray, congested voice quality, or a delay in voluntary initiation of the swallow
reflex and coughing during or after swallowing (Horner et al 1988b). Diagnosis is initially
established through clinical assessment involving an oral motor examination followed by the
introduction of one or several teaspoons of water. If patients are able to successfully swallow
this minimal amount of fluid, a small cup of water is carefully introduced. The full assessment is
described elsewhere (Smithard et al. 1996). While all stroke patients are potential aspirators,
there are certain identifiable risk factors that have been recognized as greatly increasing the
likelihood of aspiration. These clinical risk factors are below.
E1.4 Risk Factors for Aspiration Post Stroke
Q5. What are the risk factors or clinical red flags for aspiration post stroke?
Answer
1. Brainstem Stroke
2. Difficulty swallowing oral secretions
3. Coughing/throat clearing or wet, gurgly voice quality after swallowing water
4. Choking more than once while drinking 50 cc of water
5. Weak voice and cough
6. Wet-hoarse voice quality
7. Recurrent lower respiratory infections
8. Low-grade fever or leukocytosis
9. Auscultatory evidence of lower lobe congestion
10. Immunocompromised state
E1.5 Dysphagia Post Stroke
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Q6. How common is dysphagia following acute stroke?
Answer
1. The incidence of dysphagia appears to be quite high following acute stroke with between
one third and two-thirds of patients affected, depending on the population studied and the
criteria used to diagnose dysphagia.
Discussion
The majority of studies reviewed above assessed swallowing status in the acute phase of
stroke. Among these studies, the incidence of dysphagia ranged from 19% to 45%. Only two
trials (DePippo et al. 1994, Gottlieb et al. 1996) assessed swallowing upon rehabilitation to a
rehabilitation unit. The incidences of dysphagia were 61% and 28%, respectively.
E1.6 Silent Aspiration
Q7. What is silent aspiration and why is it important?
Answers
1. Silent aspiration is defined as “penetration of food below the level of the true vocal cords
without cough or any outward signs of difficulty”.
2. Important because aspiration risk may go undetected placing the patient at higher risk of
developing aspiration related complications.
3. 9-27% of acute stroke patients are silent aspirators, a condition which is only reliably
detectable through VMBS studies.
4. Between one-third to one-half of aspirators are “silent” aspirators.
Discussion
In addition to overt signs of aspiration, such as chocking or coughing, a substantial number of
patients experience silent aspiration, highlighting the utility of using VMBS studies. "Silent
aspiration" is defined as "penetration of food below the level of the true vocal cords, without
cough or any outward sign of difficulty" (Linden and Siebens 1983). Detailed clinical swallowing
assessments were shown to under-diagnose or miss these cases of aspiration (Horner and
Massey 1988a, Horner et al. 1988b, Splaingard et al. 1988, Terre & Mearin 2006). In particular,
the presence or absence of a gag reflex failed to distinguish aspirating from non-aspirating
stroke patients (Horner and Massey 1988a, Horner et al. 1988b, Splaingard et al. 1988). Silent
aspirators were considered to be at increased risk of developing complications. Since the
condition was not diagnosed, precautions to decrease aspiration risk would often not be
employed. 9 to 27% of acute stroke patients are silent aspirators, a condition which is only
reliably detectable through VMBS studies. Between one-third and one-half of aspirators are
“silent” aspirators.
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Q8. When should silent aspiration in a stroke patient be suspected?
Answer
1. Silent aspiration should be suspected in any stroke patient who presents with recurrent
lower respiratory infections, chronic congestion, a low-grade fever, leukocytosis, weak voice
or cough or a wet-hoarse voice quality after swallowing.
Discussion
Silent aspiration should be suspected in the stroke patient with recurrent lower respiratory
infections, chronic congestion, low-grade fever or leukocytosis (Muller-Lissner et al. 1982).
Clinical markers of silent aspiration may include a weak voice or cough or a wet-hoarse voice
quality after swallowing.
Canadian Stroke Strategy Guideline (2008): Recommendation 6.1 – Dysphagia
Assessment
Patients with stroke should have their swallowing ability screened using a simple, valid, reliable
bedside testing protocol as part of their initial assessment, and before initiating oral intake of
medications, fluids or food [Evidence Level B] (CSQCS, NZ, SCORE, SIGN 78).
i. Patients who are not alert within the first 24 hours should be monitored closely and dysphagia
screening performed when clinically appropriate [Evidence Level C].
ii. Patients with stroke presenting with features indicating dysphagia or pulmonary aspiration
should receive a full clinical assessment of their swallowing ability by a speech–language
pathologist or appropriately trained specialist who should advise on safety of swallowing ability
and consistency of diet and fluids [Evidence Level A] (CSQCS, NZ, RCP, SCORE).
iii. Patients who are at risk of malnutrition, including those with dysphagia, should be referred to
a dietitian for assessment and ongoing management. Assessment of nutritional status should
include the use of validated nutrition assessment tools or measures [Evidence Level C] (AU).
E1.7 Pneumonia and Aspiration Post Stroke
Q9. What is the relationship between aspiration and pneumonia?
Answers
1. Aspiration alone is not sufficient to cause pneumonia. Aspiration of small amounts of saliva
occurs during sleep in almost half of normal subjects.
2. Aspiration pneumonia is thought to occur when the lung's natural defences are
overwhelmed when excessive and/or toxic gastric contents are aspirated, leading to a
localized infection or a chemical pneumonitis.
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3. Those patients who aspirate over 10% of the test bolus or who have severe oral and/or
pharyngeal motility problems on VMBS studies are considered at high risk for pneumonia.
4. The severity of aspiration correlates with the risk of developing pneumonia.
Discussion
Aspiration alone is not sufficient to cause pneumonia. Aspiration of small amounts of saliva
occurs during sleep in almost half of normal subjects (Finegold 1991, Huxley et al. 1978).
Aspiration pneumonia is thought to occur when the lung's natural defences are overwhelmed
when excessive and/or toxic gastric contents are aspirated, leading to a localized infection or a
chemical pneumonitis. Those patients who aspirate over 10% of the test bolus or who have
severe oral and/or pharyngeal motility problems on VMBS studies are considered at high risk for
pneumonia (Logemann 1983, Milazzo et al. 1989). In many cases, it is difficult to practically
assess whether 10% or more of the test bolus has been aspirated. Nevertheless, the degree of
aspiration seen on VMBS study is a critical determinant of aspiration risk and subsequent
patient management.
The importance of the diagnosis and management of aspiration post stroke has been driven by
the purportedly causal relationship between aspiration and pneumonia (Brown and Glassenberg
1973, Hanning et al. 1989, Holas et al. 1994, Johnson et al. 1993). In turn, mortality following a
stroke as a consequence of pneumonia (presumably due to aspiration) has been reported as
high as 3% within the first 3 months (Kidd et al. 1995) and 6% within the first year (Hanning et
al. 1989). Aspiration pneumonia has therefore been regarded as important because of its
significant contribution to morbidity and mortality (Arms et al. 1974, Gordon et al. 1987, Hanning
et al. 1989, Johnson et al. 1993, Logemann 1983, Silver et al. 1984, Veis and Logemann 1985).
E1.8 Risk Factors for Aspiration Pneumonia
Q10. What are some of the risk factors for aspiration pneumonia?
Answers
1. Brainstem stroke
2. Aspiration of VMBS (risk greater if greater than 10% aspirated)
3. Aspiration of thick fluids or solids
4. Slower pharyngeal transit time on VMBS
5. Reduced levels of consciousness
6. Elderly
7. Dysarthria
8. Cognitive difficulties
9. Failure of water swallow test
Discussion
Factors associated with an increased risk of aspiration pneumonia include: dysphagia related
factors due to stroke (see Table E1), as well as reduced levels of consciousness, a
tracheostomy, gastric reflux or emesis, nasogastric tubes (due to mechanical interference with
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the cardiac sphincter), and a compromised immune system (Finegold 1991). Predicting
whether a patient will develop pneumonia post aspiration is, to some extent, dependent on other
factors such as the immune state or general health of the stroke patient. Sellars et al. (2007)
prospectively evaluated 412 stroke patients for up to 3 months following stroke. Over this
period, there were 160 cases of either confirmed or suspected pneumonias. Independent
predictors of pneumonia were age >65 years, dysarthria or no speech due to aphasia, a
modified Rankin Scale score ≥4, an Abbreviated Mental Test score <8, and failure on the water
swallow test. The presence of 2 or more of these risk factors carried 90.9% sensitivity and
75.6% specificity for the development of pneumonia.
Factors More Likely to be Associated with Aspiration Pneumonia Following Stroke




Brainstem stroke
Aspiration on VMBS (risk greater if aspirates over 10% of barium laced test material)
Aspiration of thick fluids or solids
Slower pharyngeal transit time on VMBS
References
Arms R, Dines D, Tinstman T. Aspiration pneumonia. Chest 1974; 65:136-139.
Barer DH. The natural history and functional consequences of dysphagia after hemispheric stroke. J
Neurol Neurosurg Psychiatry 1989; 52:236-241.
Bounds JV, Wiebers DO, Whisnant JP, Okazaki H. Mechanism and timing of deaths from cerebral
infarctions. Stroke 1981; 12(4):474-477.
Brown M, Glassenberg M. Mortality factors in patients with acute stroke. JAMA 1973; 224:1493-1495.
DePippo KL, Holas MA, Reding MJ, Mandel FS, Lesser ML. Dysphagia therapy following stroke: A
controlled trial. Neurology 1994; 44:1655-1660.
Finegold SM. Aspiration pneumonia. Reviews of Infectious Diseases 1991; 13(Suppl 9):S737-742.
Finestone HM, Greene-Finestone LS, Wilson ES, Teasell RW. Malnutrition in stroke patients on the
rehabilitation service at followup: prevalence and predictors. Arch Phys Med Rehabil 1995; 76:310-316.
Gordon C, Hewer RL, Wade DT. Dysphagia in acute stroke. Br Med J 1987; 295:411-414.
Gottlieb D, Kipnis M, Sister E, Vardi Y, Brill S. Validation of the 50 ml3 drinking test for evaluation of
poststroke dysphagia. Disabil Rehabil 1996; 18(10):529-532.
Hanning C, WuttgeHanning A, Hormann M, Hermann I. A cinematographic study of the pathologic
mechanism of aspiration pneumonia. Fortschv Rontgenstr 1989; 159(3):260-267.
Heart and Stroke Foundation of Ontario. Improving Recognition and Management of Dysphagia in Acute
Stroke. 2002.
Holas MA, DePippo KL, Reding MJ. Aspiration and relative risk of medical complications following stroke.
Arch Neurol 1994; 51:1051-1053.
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Horner J, Massey EW. Silent aspiration following stroke. Neurology 1988; 38:317-319(a).
Horner J, Massey EW, Riski JE, Lathrop DL, Chase KN. Aspiration following stroke: Clinical correlates
and outcome. Neurology 1988;38:1359-1362(b).
Huxley EJ, Viroslav J, Gray WR, Pierce AK. Pharyngeal aspiration in normal adults and patients with
depressed consciousness. Am J Med 1978; 64:564-568.
Johnson ER, McKenzie SW, Sievers A. Aspiration pneumonia in stroke. Arch Phys Med Rehabil 1993;
74:973-976.
Kidd D, Lawson J, Nesbitt R, MacMahon J. The natural history and clinical consequences of aspiration in
acute stroke. Quarterly J Med 1995; 88:409-413.
Linden P, Siebens AA. Dysphagia: predicting laryngeal penetration. Arch Phys Med Rehabil 1983;
64:281-284.
Logemann JA. Evaluation and treatment of swallowing disorders. San Diego, CA: CollegeHill Press,
1983.
Milazzo LS, Bouchard J, Lund DA. The swallowing process: effects of aging and stroke. Physical
Medicine and Rehabilitation: State of the Art Reviews 1989; 3(3):489-499.
MullerLissner SA, Fimmel CJ, Will N, et al. Effect of gastric and transpyloric tubes on gastric emptying
and duodenogastric reflux. Gastroenterology 1982; 83:1276-1279.
Platt J. Dysphagia Management for Long Term Care: A Manual for Nurses and Other Healthcare
Professionals. Clinical and Educational Services, Hamilton, Ont, 2001.
Scmidt EV, Smirnov VE, Ryabova VS. Results of the sevenyear prospective study of stroke patients.
Stroke 1988; 19(8):942-949.
Schmidt J, Holas M, Halvorson K, Reding M. Videofluroscopic evidence of aspiration predict pneumonia
and death but not dehydration following stroke. Dysphagia 1994; 9:711.
Sellars C, Bowie L, Bagg J, et al. Risk factors for chest infection in acute stroke: a prospective cohort
study. Stroke 2007; 38:2284-2291
Sharma JC, Fletcher S, Vassallo M, Ross I. What influences outcome of strokepyrexia or dysphagia? Int
J Clin Pract 2001; 55(1):1720.
Silver F, Norris J, Lewis A, Hachinski V. Early mortality following stroke: a retrospective review. Stroke
1984; 15(3):492-496.
Smithard DG, O'Neill PA, Park C, Morris J, Wyatt R, England R, Martin DF. Complications and outcome
after acute stroke. Does dysphagia matter? Stroke 1996; 27:1200-1204.
Splaingard ML, Hutchins B, Sulton LD, Chaudhuri G. Aspiration in rehabilitation patients:
videofluoroscopy vs bedside clinical assessment. Arch Phys Med Rehab 1988; 69:637-640.
Steele CM. Emergency room assessment and intervention for dysphagia: a pilot project. J Speech
Language Pathology and Audiology 2002; 26:100-110
Teasell RW, Bach D, McRae M. Prevalence and recovery of aspiration poststroke: a retrospective
analysis. Dysphagia 1994; 9(1):35-39.
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Teasell RW, Marchuk Y, McRae M, Finestone HM. Pneumonia associated with aspiration following
stroke. Arch Phys Med Rehabil 1996; 77:707-709.
Terre R, Mearin F. Oropharyngeal dysphagia after the acute phase of stroke: predictors of aspiration.
Neurogastroenterol Motil 2006; 18(3):200-205.
Tobin MJ. Aspiration pneumonia. In: Dantzker DR (ed). Cardiopulmonary Critical Care. New York,
Grune and Stratton, 1986.
Veis S, Logemann J. Swallowing disorders in persons with cerebrovascular accidents. Arch Phys Med
Rehabil 1985; 66:373-374.
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E2. Dysphagia Case Study
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E2. Dysphagia Case Study
E2.1 Lateral Medullary Infarction (Wallenburg’s Syndrome)
Case Study
A 68-year old man presents with a stroke involving the territory of the left lateral
medulla. This is due to an infarct of the posterior inferior cerebellar artery. The patient
presents to the Emergency Room with significant ataxia, dizziness and dysarthria.
Q1. Describe the affected vasculature and the typical presentation of a left lateral
medullary infarction (Wallenburg’s syndrome)?
Answers
Ipsilateral Side (right-side):
 Horner’s syndrome (ptosis, anhydrosis and miosis)
 Decrease in pain and temperature over ipsilateral face
 Cerebellar signs such as ataxia
Contralateral Side (left-side):
 Decreased pain and temperature over contralateral body
 Dysphagia, dysarthria, hoarseness and paralysis of vocal cord
 Vertigo, nausea and vomiting
 Hiccups
 Nystagmus, diplopia
Should not mention facial or extremity weakness.
E2.2 Assessment of Dysphagia Post Stroke
Case Study (continued)
The nurse in the emergency room provides the patient with a drink of water. The patient
responds with choking. He develops a persistent cough while in the emergency room.
Q2. What would be the next step?
Answers
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1. Having had a brainstem stroke, this patient would be considered at relatively high risk of
aspirating.
2. Acute stroke patients should be maintained NPO until their swallowing ability is determined.
3. A clinical bedside screening should be conducted by a trained team member and if there are
any concerns or the patient is regarded at risk of dysphagia than an oral motor assessment
should be performed, generally by a speech-language pathologist.
4. This trial involves 1-2 teaspoons of water and if that is well tolerated is followed by a small
cup of water.
Discussion
The Water Swallowing Test
The water-swallowing test has also been studied extensively. It has been used as both a stand
alone screening method and also as part of a clinical swallowing screening or assessment.
While the original test required a patient to swallow 3 oz (90 mL) of water, lesser amounts have
also been used. To be clinically useful, screening tests need to be valid, reliable, easy to use,
non-invasive, quick to administer (15-20 min) and pose little risk to the patient. Although many
screening tools have been developed it is unclear how many of them are used in institutions
beyond those where they were developed. Many institutions use informal processes, or simply
restrict all food and drink until complete assessment by an SLP. A wide range of sensitivities
were reported among the tools we reviewed (0% to 100%). Usually, as sensitivity increased,
specificity decreased, such that the number of patients who were incorrectly identified as
dysphagic increased. Generally screening tools with sensitivity > 80%, with a specificity that
approaches this figure are considered to be both valid and clinically useful.
The results of a systematic review by Martino et al. (2000), evaluating the screening accuracy of
49 individual clinical screening tests for orophayngeal dysphagia suggest that there is only
sufficient evidence to support the value of two tests: abnormal pharyngeal sensation and the 50
mL water-swallowing test. Both of these tests assessed only for the presence or absence of
aspiration. Their associated likelihood ratios were 5.7 (95% CI 2.5-12.9) and 2.5 (95% CI 1.73.7), respectively. Limited evidence for screening benefit suggested a reduction in pneumonia,
length of hospital stay, personnel costs and patients.
Case Study (continued)
The nurse looking after the patient on the acute floor has concerns that when given some
water the patient again chokes. The patient manages the 2 teaspoons of water without
difficulty but chokes once on a small cup of water (50ml) and his voice now has a wet,
gurgly sound to it.
Q3. Discuss management options now.
Answers
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1. Once a patient fails a screening test and it has been determined that a problem exits, a
more comprehensive assessment should follow, from which treatment options are
determined.
2. The assumption needs to be made that the patient is an aspirator and a videoscopic
modified barium swallow (VMBS) needs to be performed.
3. While the patient is waiting for the VMBS, the patient is kept NPO and an nasogastric (NG)
tube is inserted to ensure that the patient receives adequate nutrition and hydration.
Discussion
VMBS Examination
When aspiration is suspected, the videofluoroscopic modified barium swallow (VMBS) study is
often considered the "gold standard" in confirming the diagnosis (Splaingard et al. 1988). A
VMBS study examines the oral and pharyngeal phases of swallowing. The patient must have
sufficient cognitive and physical skills
to undergo testing (Bach et al. 1989). The subject is placed in the sitting position in a chair
designed to simulate the typical mealtime posture. Radio-opaque materials of various
consistencies are tested: barium impregnated thin and thick liquids, pudding, bread, and
cookies are routinely used. Various aspects of oral, laryngeal, and pharyngeal involvement are
noted during the radiographic examination (Table 15.13). The VMBS study is then followed by
a chest x-ray to document any barium, which may have been aspirated into the
tracheobronchial tree.
The VMBS assessment not only establishes the presence and extent of aspiration but may also
reveal the mechanism of the swallowing disorder. Aspiration most often results from a
functional disturbance in the pharyngeal phase of swallowing related to reduced laryngeal
closure or pharyngeal paresis. A VMBS study is recommended in those cases where
the patient is experiencing obvious problems maintaining adequate hydration/nutrition, where
concern is expressed regarding frequent choking while eating, or in the case of recurrent
respiratory infections.
While VMBS studies can be useful in analyzing the anatomic structures during swallowing and
detecting silent aspiration, there are some disadvantages: i) The procedure is relatively
complex, time consuming and resource intensive; ii) there is some exposure to small amounts
of radiation; iii) the test is not appropriate for some patients who may
have difficulty in sitting upright in a chair. The results of the test can also be difficult to interpret
and there can be significant variation among individual raters (Ramsay et al. 2003).
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Assessment of Swallowing Post Stroke at Time of Admission
Clinical Swallowing Assessment
Clinical Risk Factors (at least one):
 Brainstem Stroke
 Choking more than once while drinking 50cc of water
 Difficulty swallowing oral secretions
 Coughing/throat clearing or wet, gurgly voice quality after
swallowing water
 Weak voice and cough
 Recurrent lower respiratory infections.
Yes
No
Minimal Aspiration
(< 10 % of test bolus)
Dietary
Modification
No Aspiration
VMBS
Regular Diet
Gross Aspiration
(> 10 % of test bolus)
Enteral Tube
Feedings
E2.3 Management of Dysphagia Post Stroke
Case Study (continued)
The patient aspirates all consistencies of barium laced food on VMBS but only coughs on
the thin liquids. The video modified barium swallow shows significant aspiration due to
poor coordination of the pharyngeal phase of swallowing (>10% of the test bolus).
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Q4. Discuss management strategies.
Answers
1. The patient should not be fed by mouth and an NG tube is required for an extended period
of time.
2. At this point many centers would install a GJ tube to facilitate maintenance of nutrition and
hydration rather then wait.
Discussion
The VMBS study is still considered the "gold standard" in the diagnosis of aspiration. Those
patients who have difficulty with high volumes of thin liquids are considered to be at mild to
moderate risk of aspiration. In these cases oral feedings are regarded as appropriate. Before
deciding if a patient is a candidate for oral feeding, factors such as the patient's respiratory
status, the effectiveness of airway clearance along with the type and amount of aspirate must
first be considered (Bach et al. 1989). Aspirating more than 10% of the test bolus is generally
considered an indication for non-oral (ie. nasogastric, gastrostomy, jejunostomy tube) feedings;
however, the actual risks present with oral feedings for this group of patients have not been fully
established. Determining whether the patient actually aspirates more or less than 10% of the
test bolus is, as mentioned previously, an inexact science.
Management Strategies for Dysphagia
The Heart and Stroke Foundation Dysphagia Guidelines noted that, “a well coordinated care
plan can minimize the development of dysphagic complications, reduce length of hospital stay in
acute-care facilities and expedite access to specialized rehabilitation centers.
Dysphagia management has the following goals:
 Meeting the nutrition and hydration requirements of the stroke survivor.
 Preventing aspiration-related complications.
 Maintaining and promoting swallowing function as much as possible.
Dysphagia management strategies include the following:
 Modifying food and fluid textures to increase safety of oral intake.
 Using low-risk feeding practices and compensatory strategies to prevent complications such
as aspiration and choking.
 Monitoring oral intake to prevent dehydration.
 Supplementing the diet to maintain adequate nutrition.
 Using enteral feeding for individuals who are unable to swallow.
 Implementing swallow therapy to rehabilitate specific physiological swallowing impairments.
A speech-language pathologist should regularly monitor the status of individuals with dysphagia
to ensure that the management strategies employed remain appropriate,” (Heart and Stroke
Foundation of Ontario 2002).
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Case Study (continued)
The patient has a GJ tube installed. A second modified barium swallow is done and this
shows an improvement in the aspiration (<10% of test bolus). The patient is able to handle
pureed consistencies well but still shows aspiration on thin liquids.
Q5. Discuss management.
Answers
1. The patient can be fed orally a pureed diet with a restriction on thin liquids.
2. Fluids can be supplemented through the G-J tube.
3. Another VMBS would need to be ordered for 2-3 months and the patient carefully monitored
by a dietician and speech-language pathologist.
Discussion
Management of Gross Aspiration
Gross Aspiration
After 4-8 wks
Regular
Diet
Negative for Aspiration
Repeat
VMBS
Gross Aspiration
(> 10 % of test bolus)
Minimal Aspiration
(< 10 % of test bolus)
Dietary
Modifications
- 20 -
Continue
Enteral
Feeding
Case Study (continued)
3 months later the patient has a repeat VMBS and continues to show improvement,
although she is still having trace aspiration with thin liquids.
Q6. Discuss management.
Answers
1. The patient can continue to be fed orally an unrestricted diet.
2. However, they are advised to sip thin liquids and double cough afterwards.
3. The patient needs to continue to be monitored for a lung infection.
Discussion
- 21 -
Continuing Management of Minimal Aspiration
Minimal Aspiration
(< 10% of test bolus on VMBS)
Improved
Clinical
Swallowing
Assessment
Upgrade Diet
Modifications
Not Improved
(4-12 wks)
Negative for Aspiration
Repeat
VMBS
Regular Diet
Minimal Aspiration
(< 10 % of test bolus)
Continue or Upgrade
Dietary Modifications
References
Bach DB, Pouget S, Belle K, Kilfoil M, Alfieri M, McEvoy J, Jackson G. An integrated team approach to
the management of patients. J Allied Health 1989; 459-468.
Heart and Stroke Foundation of Ontario. Improving Recognition and Management of Dysphagia in Acute
Stroke. 2002.
Martino R, Pron G, Diamant N. Screening for oropharyngeal dysphagia in stroke: insufficient evidence for
guidelines. Dysphagia 2000; 15:19-30.
Ramsey DJ, Smithard DG, Kalra L. Early assessments of dysphagia and aspiration risk in acute stroke
patients. Stroke 2003; 34(5):1252-1257.
- 22 -
Splaingard ML, Hutchins B, Sulton LD, Chaudhuri G. Aspiration in rehabilitation patients:
videofluoroscopy vs bedside clinical assessment. Arch Phys Med Rehab 1988; 69:637-640.
- 23 -
E3. Dysphagia Case Study
- 24 -
E3. Dysphagia Case Study
Case Study
A 56-year-old right-handed hypertensive, type II diabetic was admitted to a local hospital
with complaints of occipital headache, right hand tingling, right limb ataxia, hoarse voice,
dysphagia, nausea, vomiting and vertigo. Blood pressure was elevated but weakness was
not noted on examination. He was transferred to a tertiary care center where an
occlusion of the posterior inferior cerebellar artery was diagnosed.
E3.1 Lateral Medullary Infarction (Wallenburg’s syndrome)
Q1. Describe the affected vasculature and the typical presentation of a right lateral
medullary infarction (Wallenburg’s syndrome)?
Ipsilateral Side (right-side):
 Horner’s syndrome (ptosis, anhydrosis and miosis)
 Decrease in pain and temperature over ipsilateral face
 Cerebellar signs such as ataxia
Contralateral Side (left-side):
 Decreased pain and temperature over contralateral body
 Dysphagia, dysarthria, hoarseness and paralysis of vocal cord
 Vertigo, nausea and vomiting
 Hiccups
 Nystagmus, diplopia
Should not mention facial or extremity weakness.
- 25 -
E3.2 Management of Dysphagia Post Stroke
Case Study (continued)
The following day he was noted to have severe dysphagia which was his primary complaint
and bilateral aspiration pneumonia which was confirmed on x-ray. Antibiotics were
initiated for the pneumonia. The speech language pathologist did a bedside swallowing
assessment on the day of admission. His vocal quality was described as “wet” and he could
not elevate the hyoid bone, indicating a probable swallow reflex problem. Oral motor
elevation revealed tongue elevation was significantly reduced, with a low resting soft
palate on the left and reduced movement on that side during phonation. No gag reflex
could be elicited. Mild hypernasality during conversation was noted. Maximum phonation
duration at 6 seconds indicated reduced breath support, likely resulting from vocal cord
paralysis. During phonation and conversation vocal quality was moderately breathy. He was
noted to have a weak cough and diminished throat-clearing ability. A swallow reflex could
not be elicited.
Q2. What step would you do next?
Answers
1. The next step would be to decide to do a VMBS or if not readily available, assume the
patient was a gross aspirator.
Case Study (continued)
The bedside swallow assessment therefore deemed he was unsafe for oral feeds and at
risk for the development of further aspiration. A VMBS was not performed at that time
because it was not perceived that the test would change clinical management, in view of
the severity of the results of the bedside assessment.
Initially the patient was kept NPO and a NG tube was inserted to provide nonoral feeds.
The patient was carefully followed and one week after the stroke the SLP noted evidence
of initiation of a swallow reflex. At that point, a clinical trial of both thin and thick fluids
was attempted. He continued to demonstrated clinical signs of possible aspiration, such as
coughing and a wet voice with both fluid consistencies. There was a delay in the initiation
of the swallow reflex and the patient reported marked difficulty in clearing food through
- 26 -
the pharynx. Vocal quality was wet and gurgly and there was post-swallowing coughing and
throat clearing. A head turn compensatory strategy toward the left side was attempted
to direct the bolus down the stronger side of the pharynx. The patient reported that this
seemed to only minimally help the pharyngeal clearing. Given the severity of his swallowing
problems, the apparent high risk of aspiration, and the anatomical location of his stroke, a
GJ tube was recommend and this was inserted percutaneously.
During the first month following his stroke, the patient demonstrated improvement in his
pharyngeal swallow including better clearing of oral secretions and mild improvement in
clearing of thickened fluids. He continued to use lateral head rotation to the left side
during the swallow assessment; however, there were continuing clinical signs of laryngeal
penetration of oral contents.
The patient was subsequent admitted to a stroke rehabilitation unit one month following
the onset of his stroke. Further bedside assessments indicated that he was unable to
tolerate more than half a teaspoon of thin liquids at any time. The SLP noted that the
patient likely had experienced a delay in the initiation of his pharyngeal swallow, and he
was experiencing weakness of pharyngeal peristalsis. This likely resulted in residue in the
both valleculae and pyriform sinuses. The patient was given oral and pharyngeal exercises
to be used when clearing his oral secretions to improve the strength of pharyngeal
constriction, i.e., hard glottal swallows with the head turned to the left.
Q3. What would be your next step?
Answer
1. Next step would be to conduct a repeat VMBS study (see the algorithm below).
Discussion
- 27 -
Management of Gross Aspiration
Gross Aspiration
After 4-8 wks
Regular
Diet
Negative for Aspiration
Repeat
VMBS
Gross Aspiration
(> 10 % of test bolus)
Continue
Enteral
Feeding
Minimal Aspiration
(< 10 % of test bolus)
Dietary
Modifications
Case Study (continued)
A VMBS study was subsequently performed and indicated good oral transport of all
consistencies presented. A half teaspoon of pudding revealed moderate delay in the
swallow reflex with minimal residue in the valleculae but a large residue present in the
pyriform sinus that was then grossly aspirated. Presentation of a half teaspoon of thick
liquids with the chin tucked again revealed gross aspiration occurring from a large residue
in the pyriform sinus. A second half teaspoon of thick liquids with head turned to the left
continued to show large residual in the pyriform sinus along with gross aspiration. It was
recommended that the patient continue with the GJ tube feedings exclusively. He was
receiving tube feedings from 1900 to 0800 hours and at 1200 to 1330 hours. This
schedule was designed to minimize disruption to rehabilitation therapies.
At the time of discharge from the stroke rehabilitation program almost 2 months after
his initial presentation with the stroke, the patient was close to be an independent with a
walker, requiring only minimal assistance with tub transfers and being discharged home
with the G-J tube feedings.
- 28 -
Q4. What would be the next step?
Answers
1. The next step would be to carefully follow the patient and later repeat the VMBS hoping to
get this gentleman off of the G-J tube feedings.
Case Study (continued)
A second VMBS was performed 4 months post-stroke onset. This showed that the pudding
and thick fluids still resulted in large residue being present in the pyriform sinus with
moderate to large aspiration from both. No cough was heard when he aspirated. With
thin liquids large residue was present in the pyriform sinus resulting in laryngeal
penetration and aspiration. This VMBS study indicated that he was still unsafe with
swallowing and required tube feedings. Upon laryngeal penetration of thick liquids he was
asked to cough and this cleared the penetration. A third VMBS was conducted 2 months
later (6 months post-stroke onset). Poor epiglottic motion and weak pharyngeal peristalsis
were present. It was noted that there was marked pyriform sinus residue and mild
vallecular residue with thin and thick liquid barium and pudding consistencies. Aspiration
was demonstrated with these consistencies but they did not elicit a cough. It was
recommended that he continue to be fed through the GJ tube.
Six months later (1 year subsequent to his lateral medullary stroke) this man had his
fourth VMBS study. The SLP noted a significant improvement in his swallowing. He
continued to show large residue in the valleculae and pyriform sinuses, more so in the
latter. Double swallowing with consistencies of thick liquids and pudding allowed him to
clear the residue. He was able to swallow small amounts of thin liquids, with double
swallowing, with no aspiration. He had trouble with bread and cookie consistencies.
Q5. How would you manage his swallowing problem at this stage?
Answers
1. The patient should be placed on a pureed diet with thick fluids but not allowed bread or
cookie consistencies
2. Care needs to be taken with thin liquids and it would be best to not allow him to drink thin
liquids but continue to provide additional fluid through the G-J tube.
Case Study (continued)
- 29 -
The patient was put on a pureed diet with thick fluids but was not allowed bread or cookie
consistencies. He was still maintained on GJ tube feedings primarily at need, but this was
reduced to allow for his oral feedings.
A fifth and final VMBS was performed 6 months later, more than 18 months following the
onset of his stroke. Most of the thick liquid barium was transferred into the esophagus;
however, there was impaired pharyngeal peristalsis so that after swallowing a minimal
residue remained in the valleculae and a minimum to moderate residue remained in the
pyriform sinus. No laryngeal penetration was noted. With pudding, bread, and cookie
consistencies the results were the same. With thin liquids there was occasional episodes
of trace laryngeal penetration and trace aspiration. After the swallows minimal residue
was in the valleculae and minimum to moderate residue was in the pyriform sinus. Results
with thin liquids from a cup were similar.
Q6. What would you do at this stage?
Answers
1. The patient can now be fed orally for all consistencies.
2. Care still needs to be taken with thin liquids with the patient double swallowing and throat
clearing after the fact.
3. He would need to be carefully monitored for any future episodes of pneumonia.
Case Study (continued)
It was noted that despite abnormalities in the pharyngeal phase of swallowing, there was
no laryngeal penetration or aspiration with thick fluids, pudding, bread or cookie
consistencies. It was suggested that the patient continue to use supraglottic swallowing as
well as throat clearing to remove any material that may have penetrated. It was
recommended that he be placed on a diet of thin liquids and regular solids and no further
interventions were felt to be necessary. The GJ tube was subsequently removed. At one
time during his post-stroke period, cloxacillin was ordered for a subcutaneous skin
infection around the GJ tube.
- 30 -
E4. Dysphagia Management Post Stroke in Nursing Home Patient
- 31 -
E4. Dysphagia Management Post Stroke in Nursing Home Patient
E4.1 Low-Risk Feeding Strategies
Case Study
You are asked to see an 82 year old female who had a large right hemispheric stroke 2
years previously and who is now in a nursing home. Initially, while in hospital she had
trouble with dysphagia, initially had an NG tube in place but eventually graduated to a
regular diet. She has a left spastic hemiparesis, can ambulate with a cane and the assist
of one person, does not have use of her left arm and hand, and still tends to neglect items
on the left side. She has recently suffered two episodes of pneumonia, both of which
necessitated admission to an acute care hospital.
You are able to observe her eating lunch on the day you arrive at the nursing home. Lunch
is served in a large room with a number of the nursing home residents which is regarded as
important to ensuring residents are able to regularly socialize. The patient herself is a
very slow eater and so the nursing home has kindly assigned young students to help feed
her. Initially, the patient was able to feed herself but increasingly she has come to
depend largely on help with feeding. She is provided with a regular diet. She sits in her
chair, frequently leaning back and watching patients and staff, mostly on her right side.
The students are attentive and knowing that she tires easily, they try to get her to eat as
much as possible before she asks to go back to her room. Hence, they feed her utilizing a
tablespoon until she complains of being tired at which point she is taken to her room and
allowed to lie down and rest. Her family was pleased at the attention given her to ensure
she receives adequate nutrition and a couple of times per week they will assist.
Q1. What recommendations would you make with regard to feeding strategies?
Answers
1. The patient should be in a quiet environment.
2. The patient should be sitting at a 90 degree angle with the neck in a slightly flexed forward
position.
3. The patient should be fed by seated individual at eye level with the patient.
4. The patient should be fed slowly with a teaspoon – no tablespoon.
5. The feeding assistant should assure that the patient swallows oral contents before offering
more food.
6. Once done the patient should be kept upright for a half-hour.
- 32 -
Discussion
Low-Risk Feeding Strategies for Dysphagia
The Heart and Stroke Foundation Dysphagia Guidelines noted that, “Stroke survivors should be
encouraged and assisted to feed themselves. Individuals with dysphagia who are fed are
approximately 20 times more likely to develop pneumonia than those who feed themselves
(Langmore et al. 1998). Therefore, if dysphagic individuals cannot feed themselves
independently, hand- over-hand support should be provided from an eye level position. If full
feeding assistance is necessary, it should be provided using low risk feeding strategies.
Routine use of low-risk feeding strategies can prevent serious health problems and improve the
quality of the experience for the person being fed. All health care professionals involved in
feeding dysphagic individuals should also be able to deal with emergencies, such as choking,
which may occur during feeding.” Guidelines for low-risk feeding practices are summarized in
the following Table.
Heart and Stroke Foundation of Ontario Guidelines for low-risk feeding practices (2002)















Check the food tray to ensure the correct diet type has been provided.
Ensure the environment is calm during meals and minimize distractions.
Position the stroke survivor with the torso at 90degree angle to the seating plane, aligned in
mid-position with the neck slightly flexed.
Support the stroke survivors with pillows if necessary.
Perform mouth care before each meal to remove bacteria that have accumulated on the oral
mucosa.
Feed from a seated position, so that you are at eye level with the stroke survivor.
Do not use tablespoons. Use metal teaspoons, never plastic for feeding individuals with bite
reflexes.
Use a slow rate of feeding and offer a level teaspoon each time.
Encourage safe swallowing of liquids by providing them with wide-mouth cup or glass or in a
cut-down nosey cup, which helps prevent the head from flexing backward and reduces the risk
of aspiration. Some individuals may benefit from drinking through a straw.
Ensure that swallowing has taken place before offering any additional food or liquid.
Observe the stroke survivor for any signs or symptoms of swallowing problems during and for
30 minutes after the meal.
Perform mouth care after each meal to ensure that all food debris is cleared from the mouth.
Position the patient comfortably upright for at least 30 minutes after each meal to promote
esophageal clearance and gastric emptying and to reduce reflux.
Monitor the oral intake of the stroke survivor with dysphagia: note any food items that are not
consumed and ensure that intake is adequate, especially important in individuals receiving a
thickened-liquid diet.
Document the patient’s intake, any changes in swallowing status and any self-feeding
problems.
- 33 -
References
Heart and Stroke Foundation of Ontario. Improving Recognition and Management of Dysphagia in Acute
Stroke. 2002.
Langmore SE, Terpenning MS, Schork A, Chen Y, Murray JT, Lopatin D, Loesche WJ. Predictors of
aspiration pneumonia: how important is dysphagia? Dysphagia 1998; 13(2):69-81.
- 34 -
E5. Nutritional Issues Following Stroke
- 35 -
E5. Nutritional Issues Following Stroke
Case Study
A 75- year old female suffered a small subcortical stroke resulting in dysarthria and
clumsy hand syndrome. On admission to rehabilitation 10 days following the onset of
symptoms, the patient was observed to appear thin and had only been consuming about half
of her meal trays while on the acute service. She was safe with a regular diet. A dietitian
was consulted and an assessment was completed within several days.
History: She has been living on her own for several years in a seniors apartment since her
husband died. She rarely cooks anymore but receives 4 hours a week of home-care
services and has meals provided by Wheels (an external agency) 3x/week. She does not
have a scale and is unsure if she has lost any weight over the past 6 months. She
ambulates independently but uses a category II walker for safety. She reports her
appetite is “fair”. She has no problems with nausea or vomiting.
Physical: Ht: 160 cm wt: 47 kg. (6’3”, 103.4 lbs.) Her shoulders have a squared-off
appearance. There is loss of fat in the interosseous and palmar areas of the hand.
Biochemistry: Normal Reference range included in paraentheses
Total protein - 70 g/L (60-80 g/L)
Serum albumin - 37 g/L (>35 g/L)
Serum prealbumin - 0.20 g/L (>0.18 g/L)
Serum creatinine - 4 g/L (8 to 14 g/L)
Random glucose - 6 mmol/L (<11 mmol/L)
E5.1 Body Mass Index (BMI)
Q1. What is this patient’s Body Mass Index (BMI)?
Answers
BMI or body mass index is often used to estimate whether a person is underweight, normal
weight or overweight. While there are limitations associated with the use of BMI to detect
overweight or obese individuals, it is useful to help quickly identify those who are underweight
and may be malnourished.
BMI =Weight [in kilograms] / (Height [in meters])²
BMI=47/1.602
- 36 -
BMI= 18.4
There are many interpretations of BMI although values between 19.5 and 23.5 are considered
optimum by most professionals. A BMI of 25 to 29.9 is considered overweight and one 30 or
above is considered obese. A value less than 19.5 is considered to be underweight.
E5.2 Assessment of Nutritional State
Q2. What information can be used from her history and physical to help with the
assessment of her nutritional state?
Answers
1. Based on the limited information given, we can assume that both her remote and recent
intake have been less than optimum. She has been living on her own and doesn’t cook for
herself regularly. Her oral intake while in the hospital appears to be poor. Her low BMI also
supports this finding.
2. Her physical appearance suggests evidence of both muscle wasting and fat loss.
3. The biochemical data we are given reveals few abnormalities; other than a low serum
creatinine value.
Q3. What is this woman’s nutritional status?
1. This woman presents with classic protein-energy malnutrition (PEM), or marasmus.
2. Key indicators are a low BMI, history of poor intake and a wasted appearance. It is important
to note that in this condition, there are few abnormal biochemical values. Visceral proteins,
such as albumin, frequently used to assess nutritional status, are often spared at the
expense of skeletal muscle, which is used to help meet energy requirements. The low
serum creatinine (4 g/L) suggests a loss of muscle mass, consistent with a low BMI.
Q4. Name some other nutrition assessment tools that can be used?
1. Subjective Global Assessment.
2. Mini-Nutritional Assessment.
Discussion
As we demonstrated above, nutritional status was established using all available data without
the use of a formal or structured process. This method is common in usual clinical practice. This
is largely due to the fact that there is no gold standard that has been established. Furthermore,
- 37 -
few methods of nutritional assessments have been previously validated and none have been
validated for use on patients recovering from stroke. There are two methods which have been
validated previously and have been used in published trials examining stroke. They are both
suitable for clinical use.
A traditional approach to nutritional assessment, which includes a combination of
anthropometric and biochemical measurements can also be used to determine nutritional
status, although none of these methods have been validated. Careful attention should be paid to
the limitations of the individual items that are used, and the reference ranges and cut-off limits
that are chosen.
Other, more sophisticated techniques such as bioelectrical impedance analysis, whole body
counts (of Potassium, Nitrogen, Phosphorous, Oxygen etc) can also be used to estimate body
cell mass and fat free mass, but they are usually reserved for research purposes. Functional
measures including grip strength, respiratory muscle strength and muscle fatigue tests are also
rarely used in a clinical setting to assess nutritional state.
Q4-1. Describe the SGA.
Answer
The SGA is a method of nutritional assessment that was designed for use in the prediction of
risk for complications following general surgery, based on pre-operative nutritional state (Detsky
et al. 1987).
Discussion
Questions
What does it
measure?
What is the scale?
What are the key
scores?
What are the
strengths?
What are the
limitations?
Answer
Nutritional status
Two part clinical assessment
History: focus on weight loss, edema, anorexia, vomiting,
diarrhea, decreased food intake, chronic illness
Physical exam: focus on jaundice, glossitis, cheilosis, loss of
subcutaneous fat, muscle wasting, edema
Patients were classified as normally nourished (A), mildly
malnourished or suspected of being malnourished (B) or
severely malnourished (C) based subjective assessment
Quick, non-invasive, inexpensive
Specialized training required. Poor reliability due to subjective
nature of the items assessed.
Q4-2. Describe the MNA
- 38 -
Answer
The MNA was developed as a screening and assessment tool to identify geriatric patients at risk
for malnutrition (Guigoz et al. 1994).
Discussion
Questions
What does it
measure?
What is the scale?
What are the key
scores?
Answer
Nutritional status-may be used for both screening and
assessment
18 items including
Anthropometric measurements
Global assessment (6 questions related to lifestyle, medication
& mobility)
Dietary questionnaire
Subjective assessment (self-perception of health and nutrition)
Screening: scores < 12 possible malnutrition
Sub total maximum score 14
Assessment: Scores < 17 indicates malnutrition
Scores of 17 to 23.5 indicates at risk of malnutrition
Sub total maximum score 16
Maximum score: 30
What are the
strengths?
What are the
limitations?
Provides prognostic information
Time-consuming to perform (about 20 minutes) Dependent on
subject’s ability to answer questions related to their diet history
E5.3 Protein and Energy Requirements
Q5. What are this patient’s protein and energy requirements?
Answers
There are a number of different methods to estimate energy requirements. One of the most
commonly used is the Harris Benedict equation, which estimates resting energy requirements
using a patient’s height, weight and age
M: 66.5 +13.8(W) + 5 (H) - 6.8 (age) = Kcal/day
F: 655 + 9.6 (W)+1.8 (H) - 4.7 (age) = Kcals/day
This patient would require 1,047 Kcals/day
655 + 9.6 (103) + 1.8 (63) – 4.7 (75)
A stress factor of 1.2 combined with an activity factor of 1.2 are used to estimate the total
amount of energy required for repletion
- 39 -
1,047 x 1.2 x 1.2 = 1,508 Kcals/day
A simpler method of estimating energy intake is to use a standard requirement of 35 Kcals/kg
35 Kcals/day x 47 kg = 1,645 Kcals/day to achieve weight gain
Protein requirements are estimated to be 1-1.2 g/kg/day (47-56 g/day).
Q6. What diet would you recommend for this patient? What are the goals of treatment?
Answers
1. Given that this woman appears to be suffering from uncomplicated malnutrition and does
not require dietary restrictions due to dysphagia or co-morbidities, a high calorie, high
protein diet is indicated.
2. Weight gain is the goal of treatment.
Discussion
Given that this woman appears to be suffering from uncomplicated malnutrition and does not
require dietary restrictions due to dysphagia or co-morbidities, a high calorie, high protein diet is
indicated. Oral supplements and/or high energy/protein snacks should be included. Oral
supplements come in many flavours and forms including liquids, bars and puddings.
Supplements may be given at mealtime along with reduced portions, or between meals. Most
oral supplements contain approximately 250 to 300 Kcal and 8 to 13 g of protein per 250-mL
serving.
Calorie counts should be initiated to ensure that she consumes sufficient energy and protein.
Weight gain is the goal of treatment. If she consumes her estimated requirements daily, she
should achieve a weight gain of 1 to 2 lbs per week.
Gariballa et al (1998) demonstrated that malnourished stroke subjects receiving oral
supplements that provided an additional 600 Kcals/day and 20 g protein had significantly higher
energy and protein intakes compared to subjects who consumed a regular hospital diet. At the
end of follow-up (12 weeks), subjects in the supplement group had gained an average of 0.2 kg
compared to subjects in the control group who had lost an average of 0.7 kg.
Q7. How who you monitor and assess the progress?
Answers
1. Weekly weights should be obtained for the duration of the inpatient stay.
2. Calorie counts should be continued intermittently to ensure that adequacy of intake is
maintained.
- 40 -
Reference
Chicago Dietetic Association, South Shore Suburban Dietetic Association and Dietitians of Canada.
th
Manual of clinical dietetics. 6 ed. Chicago:American Dietetic Association.
Detsky AS, McLaughlin JR, Baker JP, et al. What is subjective global assessment of nutritional status?
JPEN 1987; 11:8-13
Gariballa SE, Parker SG, Taub N, Castleden CM. A randomized, controlled, a single-blind trial of
nutritional supplementation after acute stroke. J Parenter Enteral Nutr 1998; 22:315-319.
Gibson RS. Principles of Nutritional Assessment. New York, Oxford University Press, 1990.
Guigoz Y, Vellas B, Garry P. The Mini Nutritional Assessment: A practical assessment tool for grading the
nutritional state of elderly patients. Facts Res Gerontol 1994; 4:15-59.
- 41 -
E6. Deep Venous Thromboembolism
- 42 -
E6. Deep Venous Thromboembolism
Canadian Stroke Strategy Guidelines 2008: Recommendation 4.2a – Venous
Thromboembolism Prophylaxis
All stroke patients should be assessed for their risk of developing venous thromboembolism
(including deep vein thrombosis and pulmonary embolism).
Patients considered as high risk include patients with inability to move one or both lower limbs
and those patients unable to mobilize independently.
i. Patients who are identified as high risk for venous thromboembolism should be considered for
prophylaxis provided there are no contraindications [Evidence Level B] (ESO).
ii. Early mobilization and adequate hydration should be encouraged with all acute stroke patients
to help prevent venous thromboembolism [Evidence Level C] (AU, ESO, SCORE).
iii. The use of secondary stroke prevention measures, such as antiplatelet therapy, should be
optimized in all stroke patients [Evidence Level A] (ASA, AU, NZ, RCP, SIGN 13).
iv. The following interventions may be used for patients with acute ischemic stroke at high risk of
venous thromboembolism in the absence of contraindications:
a. low molecular weight heparin (with appropriate prophylactic doses per agent) or heparin in
prophylactic doses (5000 units twice a day) [Evidence Level A] (ASA, AU, ESO);
b. external compression stockings [Evidence Level B] (AU, ESO).
v. For patients with hemorrhagic stroke, nonpharmacologic means of prophylaxis (as described
above) should be considered to reduce the risk of venous thromboembolism [Evidence Level C].
Case Study
A 75 year-old man presents to the Emergency-Room with left hemiplegia, due to a right
MCA stroke. 48 hours later the nurse alerts you to the fact that his left leg shows signs
of swelling and erythema.
Q1. What do this patient’s symptoms suggest?
Answer
1. This patient is showing signs of deep venous thrombosis (DVT).
2. The clinical features of DVT are present in less than half of patients with this condition.
- 43 -
E6.1 Incidence of Venous Thromboembolism in Stroke
Q2. Describe the incidence and impact of DVT in the stroke population in the absence of
prophylaxis.
Answers
1. In the absence of prophylaxis, over 60% of dense hemiplegics develop DVTs, 9-15% suffer
a pulmonary embolus, with a 1-2% mortality rate (Sioson et al. 1988).
2. In the acute phase, in the absence of prophylaxis the incidence is 50%.
3. Most are below the knee, asymptomatic and unlikely to lead to a pulmonary embolus.
4. Peak onset is 2 to 7 days post stroke.
5. The incidence of DVT on rehabilitation is less than 10% in the rehabilitation phase in the
absence of prophylaxis.
Discussion
In the absence of prophylaxis, over 60% of dense hemiplegics develop DVTs, 9-15% have
pulmonary emboli, with a 1-2% mortality rate (Sioson et al. 1988). Indeed, pulmonary embolism
has been reported to be the fourth most cause of death in the 30 days following stroke, while
the risk of thromboembolism still persists thereafter.
Studies of patients with acute hemiplegic stroke have shown a DVT incidence of approximately
50% within 2 weeks in the absence of heparin prophylaxis. The majority of DVTs affect the
paralyzed leg and are asymptomatic. Further, approximately two thirds of DVTs are below the
knee, in contrast to symptomatic DVTs, in whom the majority are proximal. 20% of distal DVTs
extend into the proximal veins. Furthermore, over 80% of symptomatic DVTs involve the
popliteal or more proximal veins. Peak onset for the development of DVT is between the
second and seventh day after the onset of stroke. DVT is also present in a significant
proportion of patients during the rehabilitation phase of stroke but with lower prevalence (1240%) and incidence (less than 10%).
E6.2 Risk Factors for Venous Thromboembolism Post Stroke
Q3. The nurse asks you how one can tell which patients are at risk for developing a
DVT?
Answers
1. Risk factors include degree of lower limb paralysis, older age, reduced consciousness,
obesity, previous DVT and atrial fibrillation.
Discussion
- 44 -
High risk patients have been identified as having lower limb plegia, reduced consciousness,
obesity and having a previous DVT (Imberti and Prisco 2005). The risk of DVT correlates with
the degree of paralysis and is greater in older patients as well as those who have atrial
fibrillation. Predilection for the paralyzed leg is probably explained by a combination of loss of
the calf muscle pump and repeated minor trauma.
E6.3 Diagnosis of Deep Venous Thrombosis
There are few ways to know the pretest probability of having a DVT, one of which is the Wells
scale. Using this scale (see table below), you can determine if a patient has a high (3 or more
points), moderate (1 or 2 points), or low (0) pretest probability for developing a DVT.
Clinical Model for Predicting Pretest Probability for Deep-vein Thrombosis
Clinical Feature
Score
Active cancer (treatment ongoing or within previous 6 months or palliative)
1
Paralysis, paresis, or recent plaster immobilization of the lower extremities
1
Recently bedridden for more than 3 days or major surgery, within 4 weeks
1
Localised tenderness along the distribution of the deep venous system
1
Entire leg swollen
1
Calf swelling by more than 3 cm when compared with the asymptomatic leg
1
(measured 10cm below tibial tuberosity)
Pitting oedema (greater in the symptomatic leg)
1
Collateral superficial veins (non-vericose)
1
Alternative diagnosis as likely or greater than that of deep-vein thrombosis
-2
Note: In patients with symptoms in both legs, the more symptomatic leg is used.
Q4. What diagnostic tests would you initially use to confirm a clinical suspicion of a
DVT? Describe briefly the role of each.
Answers
1. D-Dimer Assay: D-dimers are fibrin degredation products. Very sensitive but lacks
specificity.
2. Venous Ultrasound: Test is nonivasive and can do serial testing; sensitivity 95% for
proximal DVTs and 73% for distal DVTs.
Discussion
Venous Ultrasound
Ultrasound has a sensitivity of 95% in patients with symptomatic proximal DVT and 73% for
distal DVT. Although the majority of DVTs that extend do so within the first week, serial testing
may be used if the test is negative but the patient remains symptomatic.
D-Dimer Assay
- 45 -
This is a rapid, noninvasive and relatively inexpensive test. Fibrin is the main component of
thrombus formation and fibrin degredation products include d-dimers. Consequently, D-dimers
are frequently in the blood when venous thromboembolism is present. The positive d-dimer test
is very sensitive but lacks specificity since d-dimers are also found in other disease states,
including cancer, congestive heart failure and inflammatory conditions. In other words, one can
relax when results are negative because D-dimer assays have a high negative predictive value
(high sensitivity) but, when results are positive, the predictive value is poor because the
presence of D-dimers could be caused by something other than deep venous thrombosis (poor
specificity).
Q5. How can you make a definitive diagnosis of a DVT?
Answer
1. Venography
2. MRI
Discussion
Venography
Although venography is considered the definitive test for DVT, it is an invasive test in which
contrast dye is injected into the legs veins. Diagnosis is made if an intraluminal-filling defect is
noted.
A positive diagnosis of a DVT can only be made if the venogram is positive or there is a positive
venous ultrasound at two or more sites of the proximal veins. A negative diagnosis for DVT can
be made if there is a negative venogram, a negative d-dimer test, or a normal venous
ultrasound assuming the venous ultrasound is accompanied by one of the following findings: 1)
normal d-dimer test, 2) low clinical suspicion for DVT, 3) normal serial testing with testing
conducted one week later.
E6.4 Prevention of Deep Venous Thrombosis Post Stroke
Q6. What is the evidence for preventive pharmacological treatments for DVT
recommended in ischemic strokes?
Answers
1. There is strong evidence that prophylactic anticoagulation significantly reduces the
incidence of deep venous thromboembolism, as compared to placebo.
2. Although there is a slightly higher risk of intracerebral hemorrhage, the benefit of prophylaxis
far outweighs the risk.
- 46 -
Q7. The nurse wants to know which pharmacological agents are recommended for DVT
prophylaxis?
Answer
1. There is strong evidence that low molecular weight heparin is more effective with less risk of
hemorrhagic complications than unfractionated heparin.
2. Warfarin is an effective anticoagulant but is less reliable, more cumbersome to use and has
more bleeding complications than LMW heparin for prophylaxis.
Discussion
Unfractionated Heparin
Unfractionated heparin has immediate onset of action, must be given parenterally, and its
effects can be reversed rapidly. Bleeding is the most common adverse effect while
osteoporosis and thrombocytopenia are uncommon side effects. Heparin inactivates thrombin
and anti-thrombin and hence is non-specific in its action. It means it is also very individual
specific. In 2 RCTs of acute stroke patients, low-dose unfractionated heparin (5,000 units s/c
q8h) reduced the rate of DVT from 73-75% in the placebo group to 13-22% in the treatment
group. There are no studies of prophylaxis in subacute or rehabilitation stroke patients.
However, it’s accepted use is to maintain while at high risk (i.e. bedridden, in a wheelchair,
paralysis). There is no accepted stop date although the trend is for longer and more frequent
use.
Low Molecular Weight Heparin (LMWH)
The clinical advantages of LMWH include predictability, dose-dependent plasma levels, a long
half-life, and less bleeding for a given anthitrombotic effect. It has become more popular in the
treatment of DVT because it reduces the hemorrhagic complications. LMWH is administered
once or twice daily, both during the high-risk period when prophylaxis for DVT is recommended
and also while waiting for oral anticoagulation to take effect in the treatment of DVT. LMW
heparin has a quantifiable and predictable anticoagulant effect. It does not inactivate thrombin
but does inactivate anti-thrombin. LMW heparin drugs include:
 Daltaperin (Fragmin) 5,000 units daily
 Tinzaparain (Innohep) weight adjusted or 4,500 units daily
 Enoxaparin (Lovenox) 30 mg BID or 40 mg daily
LMW heparin is easy to administer, there is no need to monitor and patient appear to prefer it
when monitoring is required.
There are 5 RCTs comparing LMW heparin to placebo. 3 of the RCTs were positive and 2 were
of no difference. A meta-analysis of 1900 stroke patients found significant difference (23 DVTs
in Rx-group and 45 in placebo, p=0.04). There is an associated dose-dependent risk of intraand extra-cranial hemorrhage with UFH. Evidence not definitive but LMW heparin appears to
have more specific action with lower rates of hemorrhage than UFH.
- 47 -
Studies Evaluating Low Molecular Weight Heparin vs. Unfractionated Heparin
Author, Year,
n at
Treatments
Results
PEDro Score
randomization
Turpie et al. 1992
Low molecular-weight heparin vs. UFH
87
+ (LMWH)
7
heparin
Dumas et al. 1994
Low molecular-weight heparin vs.
179
8
standard heparin
Hillborn et al. 2002
Low molecular-weight heparin vs. UFH
212
+ (LMWH)
8
heparin
PROTECT 2006
Low molecular-weight heparin vs. UFH
272
ns
heparin
PREVAIL 2007
Low molecular-weight heparin vs. UFH
1762
+ (LMWH)
ns
heparin
+ Indicates a reduction in the incidence of DVT compared to placebo/alternative treatment
- Indicates no difference in the incidence of DVT compared to placebo/alternative treatment.
Forest Plot of the Effectiveness of Heparin or LMW Heparin vs. Placebo in Preventing
DVT Following Stroke
Advantages and Disadvantages of Heparin Use
Advantages
Disadvantages
 Acts immediately
 Poor sc bioavailability when given in low doses
 Proven Efficacy in high risk
 Short half-life
patients
 Repeated injections
 Can be neutralized
 Risk of thrombocytopenia (minimal with prophylaxis)
 Reference drug
 Risk of bleeding (minimal)
 Not sufficiently effective in very high risk groups
- 48 -
Warfarin
Warfarin s the most widely prescribed oral anticoagulant. An international Normalized Ratio
(INR) of 2.0-3.0 is sufficient for prophylaxis and treatment of venous tromboembolism while
minimizing the risk of haemorrhage associated with higher INRs. The anthitrombotic effect of
warfarin or the inability to expand and form clots is not present until approximately the fifth day
of therapy; therefore, concomitant use of heparin is usually required during the transition in
therapy.
Advantages and Disadvantages of Warfarin Use
Advantages
 Oral administration
 Proven Efficacy
Disadvantages





Risk of bleeding
Delayed onset of action
Delayed neutralizing
Frequent monitoring necessary
Many drug interactions
Conclusions re Anticoagulation and Prevention of DVT Post Stroke
1. There is strong evidence that anticoagulation significantly reduces the incidence of DVT
when compared to placebo.
2. There is strong evidence that LMW heparin is better than UF heparin for reducing
hemorrhagic complications associated with anticoagulant therapy and decreasing the
frequency of venous thromboembolism.
Q8. A resident asks you about the use of mechanical methods for preventing DVT, what
can you tell them?
Answers
1. There are two physical forms of prophylaxis for DVT: graded compression stockings and
intermittent pneumatic calf compression devices.
2. For both types, there is a moderate level of evidence that they are ineffective at reducing the
risk of developing DVT.
- 49 -
DVT Assessment Algorithm
Probability: Wells Score
DVT unlikely
(score < 2)
DVT likely
(score > 2)
D-dimer
D-dimer
-
+
DVT
excluded
Ultrasound
+
DVT
-
Ultrasound
Ultrasound
+
-
DVT
excluded
+
-
DVT
excluded
+
Serial US/
Venography
DVT
DVT
excluded
DVT
+
DVT
Treat
Compression
Stockings
LMWH
E6.5 Pulmonary Embolism
Case Study (continued)
You receive another call from the nurse who tells you that the patient is now experiencing
chest pain, shortness of breath, and is not interested in participating in rehabilitation
therapies.
Q9. What is the most likely diagnosis and how common is it in the stroke population?
Answer
1. Most likely a pulmonary thromboembolism
2. Relatively common following a stroke with leg paresis
3. Most severe and fatal PEs occur at 2-4 weeks post stroke.
- 50 -
Discussion
The patient is showing signs of pulmonary thromboembolism (PE), which may be a medical
emergency: Pulmonary emboli account for 13% to 25% of early deaths after stroke and it has
been reported that it is the fourth most common cause of death within 30 days after stroke.
Although they may occur as early as the third day post-stroke, fatal emboli are unusual in the
first week, occurring most frequently between the second and fourth weeks, which is when they
are most likely to be fatal. Patients who are more severely disabled are the most likely to be
affected but PE may also occur in ambulatory patients.
The signs and symptoms of PE are varied and non-specific, which often leads to difficulties with
diagnosis. The signs of PE can include sudden chest pain, shortness of breath, difficulty
breathing or rapid breathing, coughing up blood, loss of consciousness, Tachycardia, pleural
friction rub, and fever. Many cases are clinically silent with only 30% having the clinical features
of DVT and only 70% demonstrating a DVT on venography. In most cases there are only a few
clinical findings and a non-specific presentation with the major clinical complaints being malaise
and fever.
Q10. The nurse asks you how she can tell which patients are at risk for developing a PE?
Answer
1. Factors which predispose to development of pulmonary embolism are the presence of a
deep venous thrombosis, a paralyzed and immobile leg, failure to prophylactically treat with
LMW heparin, previous DVT or PE and other risk factors such as cancer.
Discussion
There are a few ways to assess the pretest probability of having a PE, one of which is the Wells
scale.
Criteria for the Calculation of the Wells Score
Criterion
Clinical signs of DVT
Alternative diagnosis less probable than PE
Heart rate > 100 bpm
Immobilization or surgery < 4 weeks ago
Previous DVT or PE
Haemoptysis
Cancer
Points Value
+3
+3
+1.5
+1.5
+1.5
+1
+1
According to this scale, a total score of < 2 indicates a low probability or PE; 2-6 indicates a
moderate probability of PE; > 6 indicates a high probability of PE.
- 51 -
Q11. How would you make the diagnosis of Pulmonary Thromboembolism?
Answers
1. Diagnosis is most often made with ventilation-perfusion scanning and/or spiral CT scanning.
Discussion
Ventilation/Perfusion Scaning
A normal perfusion scan excludes PE but perfusion defects are non-specific with only about one
third of those with defects actually having a PE. The probability that a perfusion defect is a PE
increases with the size, shape, and number of defects as well as the presence of a normal
ventilation scan.
Probability of pulmonary embolism based on ventilation-perfusion scan results and
clinical suspicion in PIOPED study
Clinical suspicion pf pulmonary embolism*
Ventilation-perfusion scan results
Low
Intermediate
High
High probability
56%
88%
96%
Intermediate probability
16%
28%
66%
Low probability
4%
16%
40%
Normal/near-normal probability
2%
6%
0%
Adapted from the PIOPED investigators (Gill and Nahum 2000, PIOPED Investigators 1990).
* Percentage of patients with pulmonary embolism
Pulmonary Angiography
A PA is the definitive diagnosis for PE. It is used when the V/Q scan is non-diagnostic but the
clinical suspicion remains high. It is an expensive test that is associated with significant risk
complications.
Spiral CT Scan
A quick spiral CT scan can scan the entire thorax in a single breath-hold. The sensitivity of this
scan ranges from 64-93% and its specificity ranges from 89-100%.
- 52 -
PE algorithm
Wells Scale
Low
Moderate / High
D-dimer
D-dimer
-
+
PE
excluded
Normal
V/Q
CTscan
No-high
Ultrasound
-
+
V/Q
CTscan
High
Normal
No-high
Ultrasound
High
Ultrasound
-
-
+
D-dimer
PE
excluded
Treat
Pulmonary
Angiography
(PA)
-
+
PA or US in 1 week
(only US for moderate
Wells score)
PE excluded
+
Treat
Case Study (continued)
The patient has been treated with warfarin and during the visit you notice that he is both
less alert and slower to respond than he has been during previous visits. The
physiotherapist also mentions that he was very difficult to work with that day.
Q12. What would you be concerned with considering the patient is being
anticoagulated?
Answer
1. Sudden change in a patient on anticoagulation is always a concern. Bleeding is the main
complication and with decreased alertness an intracranial hemorrhage is a possibility.
- 53 -
2. A CT scan should be ordered to rule out intracranial bleeding.
Discussion
It is important to consider secondary effects when you are treating a patient with anticoagulants.
For example, Hemorrhage risk is well described in patients taking warfarin. In addition to
intracranial haemorrhage, extracranial sites such as the gastrointestinal tract, genitourinary
tract, and soft tissue are common sites for hemorrhage. Patients who have had previous
hemorrhagic events while receiving warfarin are also at increased bleeding risk. Other risk
factors include liver and renal disease, hypertension, cancer, and stroke. Regarding this
patient, you must order a CT scan in order to search for intracranial bleeding.
Case Study (continued)
The CT shows a new small intracerebral haemorrhage. The warfarin is discontinued.
Q13. The resident asks you how long you should wait before restarting anticoagulation
therapy after a warfarin-associated intracerebral haemorrhage.
Answer
1. Once the patient has stabilized consideration should be given to restarting the Warfarin,
particularly if there is an ongoing risk of PE recurrence.
2. Decisions need to be made on a patient-by-patient basis. Factors which need to be taken
into consideration are the general health of the patient, age, risk of falls and ongoing risk of
PE recurrence.
Discussion
Recurrent primary ICH after reinstitution of warfarin therapy occurs less frequently than does
recurrent thromboembolic events in patients who do not restart warfarin therapy. However,
reinitiating anticoagulation therapy has been found to be associated with an increased risk of
intracerebral haemorrhage and extracranial hemorrhagic complications (Classen et al. 2008).
After an episode of WAICH, the clinician deciding whether to restart anticoagulation therapy
should weigh several factors, including the patient's risk of falls, general medical condition, and
other risk factors for systemic hemorrhage. Patients without these risks may benefit from
reinstitution of warfarin therapy as failure to do so might unnecessarily subject them to
thromboembolic complications.
References
Classen DO, Kazemi N, Zubkov AY, Wijdicks EF, Rabinstein AA. Restarting anticoagulation therapy after
warfarin-associated intracerebral hemorrhage. Arch Neurol. 2008; 65(10):1313-8.
- 54 -
Diener HC, Ringelstein EB, von Kummer R et al. Prophylaxis of thrombotic and embolic events in acute
ischemic stroke with the lowmolecular-weight heparin certoparin: results of the PROTECT Trial. Stroke
2006; 37:139-144.
Dumas R, Woitinas F, Kutnowski M, Nikolic I, Berberich R, Abedinpour F, Zoeckler S, Gregoire F,
Jerkovic M, Egberts JFM, Stiekema JCJ. A multicentre, double-blind, randomized study to compare the
safety and efficacy of once-daily ORG 10172 and twice-daily low-dose heparin in preventing deep-vein
thrombosis in patients with acute ischaemic stroke. Age Ageing 1994; 23:512-516.
Gill P, Nahum A. Improving detection of venous thromboembolism: new technology holds promise for
early, precise diagnosis. Postgrad Med 2000; 108(4):24-40.
Hillbom M, Erila T, Sotaniemi K, Tatlisumak T, Sarna S, Kaste M. Enoxaparin vs heparin for prevention of
deep-vein thrombosis in acute ischaemic stroke: a randomized, double-blind study. Acta Neurol Scand
2002;106(2):84-92.
Imberti D, Prisco D. Venous thromboembolism prophylaxis in medical patients: future perspectives.
Thromb Res 2005; 116(5):365-375.
Kay R, Wong KS, Yu YL et al. Low-molecular weight heparin for the treatment of acute ischemic stroke.
N Engl J Med 1995; 333:1588-1593.
McCarthy ST, Turner J. Low-dose subcutaneous heparin in the prevention of deep-vein thrombosis and
pulmonary emboli following acute stroke. Age Aging 1986; 15:84-88.
McCarthy ST, Turner JJ, Robertson D, Hawkey CJ, Macey DJ. Low-dose heparin as a
prophylaxis against deep-vein thrombosis after acute stroke. Lancet 1977; 11:800-801.
PIOPED Investigators. Value of the ventilation/perfusion scan in acute pulmonary embolism: results of
the prospective investigation of pulmonary embolism diagnosis (PIOPED). JAMA 1990; 263(20):27532759.
Prins MH, Gelsema R, Sing AK, Van Heerde LR, den Ottolander GJH. Prophylaxis of deep venous
thrombosis with a low-molecularweight heparin (Kabi 2165/Fragmin) in stroke patients. Haemostasis
1989;19:245-250.
Sandset PM, Dahl T, Stiris M, et al. A double-blind and randomized placebo-controlled trial of lowmolecular-weight heparin once daily to prevent deep-vein thrombosis in acute ischemic stroke. Seminars
in Thrombosis and Hemostasis 1990; 16:25-33.
Sherman DG, Albers GW, Bladin C et al. The efficacy and safety of enoxaparin versus unfractionated
heparin for the prevention of venous thromboembolism after acute ischaemic stroke (PREVAIL Study): an
openlabel randomised comparison. Lancet 2007; 369:1347-1355.
Sioson ER, Crowe WE, Dawson NV. Occult proximal deep vein thrombosis: Its prevalence among
patients admitted to a rehabilitation hospital. Arch Phys Med Rehabil 1988; 69:183-185.
Turpie AG, Gent M, Cote R, Levine MN, Ginsberg JS, Powers PJ, Leclerc J, Geerts W, Jay R, Neemeh J.
A low-molecular-weight heparinoid compared with unfractionated heparin in the prevention of deep vein
thrombosis in patients with acute ischemic stroke. Ann Intern Med 1992; 117(5):353-357.
Turpie AGG, Levine MN, Hirsh J, Carter CJ, Jay RM, Andrew M, Magnani HN, Hull RD, Gent
M. Double-blind randomised trial of ORG 10172 low-molecular-weight heparinoid in prevention of deepvein thrombosis in thrombotic stroke. Lancet 1987; 1:523-526.
- 55 -
Usefulness of a low molecular weight heparinoid in improving outcomes at 7 days and 3 months after
stroke – results of the trial of Org 10172 in acute stroke treatment (TOAST). Stroke 1998; 29:286-286.
- 56 -
E7. Venous Thromboembolism Case Study
- 57 -
E7. Venous Thromboembolism Case Study
E7.1 Prophylaxis of Venous Thromboembolism Post Intracerebral Hemorrhage
Case Study
36 year old male admitted to stroke rehabilitation program and discharged 6 weeks later.
5 weeks previously he had suffered an intracerebral hemorrhage with right sided
weakness. CT scan revealed a bleed in the left putamen and both caudate heads with
compression of the ventricles. Etiology of the bleed was felt to be related to
hypertension.
Q1. You know that the patient has a high risk for developing DVT, the nurse and the
resident want to know if patients should be prophylactically anticoagulated after
intracerebral hemorrhage?
Answer
The patient can be initiated on a typical LMW heparin prophylactic regimen without concern
about increasing the size of the intracerebral hemorrhage.
Discussion
Eckman et al. (2003) try to answer this question. They used a Markov state transition decision
model stratified by location of hemorrhage (lobar or deep hemispheric) and the effectiveness
was measured in quality-adjusted life years (QALYs). Mark et al. (2003) found that for patients
with prior lobar ICH, withholding anticoagulation therapy was strongly preferred, improving
quality-adjusted life expectancy by 1.9 QALYs. For patients with prior deep hemispheric ICH,
withholding anticoagulation resulted in a smaller gain of 0.3 QALYs. In sensitivity analyses for
patients with deep ICH, anticoagulation could be preferred if the risk of thromboembolic stroke is
particularly high.
Wasay et al. (2008 concluded that subcutaneous heparin in doses of 2500-5000 units twice
daily during the acute phase in patients with ICH may be safe for DVT prophylaxis. However, it
was not superior to elastic stockings in a non-randomized comparison to prevent DVT.
Subcutaneous heparin use in acute ICH was tested in a randomised controlled trial in which
5000U TID was started at 2, 4 and 10 days post-ictus (?REFERENCE). Treatment initiation on
day 2 significantly reduced the frequency of deep venous thrombosis, with no concomitant
increase in haematoma expansion.
- 58 -
Q2. Do you know of any other methods to prevent DVT in hemorrhagic strokes instead
of pharmacological management?
Answer
There is moderate evidence that a combination of graded compression stockings and
intermittent pneumatic devices reduce the risk of development of asymptomatic DVTs in
patients with hemorrhagic stroke.
Discussion
Prevention of DVT Through Mechanical Methods
The use of physical forms of prophylaxis, including graded compression stockings (GCS) or
TEDS has been questioned and debate continues over the risks and benefits of this treatment
for stroke patients. The mechanism by which TED stockings reduce the risk of DVT is not
entirely well-understood (Amaragiri and Lee 2000). Graduated compression stockings
compresses the surface veins, keeping their diameter small, and forcing blood into the deep
vein system. GCS can accelerate the velocity at which the blood flows through the deep veins,
which helps to relieve the symptoms associated with venous insufficiency. Although seen as a
relatively benign intervention, their use has been associated with side effects as serious as skin
ulceration and necrosis. A Cochrane review by Amaragiri and Lee (2000) suggests that there is
a significant decrease in DVT risk among post-surgical patients who wore the stockings,
although an RCTs involving stroke patients was not included in this review (Muir et al. 2000).
Mazzone et al. (2004) authored a Cochrane meta-analysis and reported on the effectiveness of
compression stockings and intermittent pneumatic compression devices among RCTs
investigating stroke patients specifically. The review included only two small RCTs, both of
which had follow-up periods of 10 days or less. The authors concluded that there was
insufficient evidence to support the use of physical methods in routine DVT prophylaxis. A
recent review by Andre et al. (2007) also suggests that there is insufficient evidence to suggest
that either elastic stockings or IPC devices are effective means to reduce DVT. The results from
the CLOTS (Clots in Legs Or TEDS after Stroke) Trial is pending. Neither Muir et al. (2000) or
Prasad et al. (1982) reported differences in the development of DVT between groups in their
small studies evaluating two different treatment approaches.
The prevention of DVT among patients suffering from ICH can be problematic given that
traditional anticoagulants are hazardous to patients already at increased risk for bleeding
complications. The VICTORIAh investigators found that a combination of TED stocking and IPC
was more effective than TED stockings alone for preventing asymptomatic DVT. There were no
cases of symptomatic DVT in either group during the study period. However, a significant
percentage (19%) did not tolerate treatment with ICP well and stopped using it within 5 days.
E7.2 Prevention of Recurrent Pulmonary Emboli in Intracerebral Hemorrhage
Case Study (continued)
- 59 -
Six days after presenting with an intracerebral hemorrhage, the patient was diagnosed
with a symptomatic DVT and a symptomatic pulmonary embolus.
Q3. The patient has developed a PE in association with an intracerebral bleed. What do
you do now?
Answer
This patient should not be anticoagulated but the risk of PE recurrence; it is necessary to insert
a vena cava filter.
Discussion
Another method to prevent PE is the vena cava filter. These filters are inserted in the vena cava
to prevent the passage of emboli into the lungs. Some reports have demonstrated success
rates as high as 96% in the prevention of PE (Greenfield and Michna 1988); however, vena
cava filters are also associated with some risk. For example, they can become blocked or
dislodged, both of which can increase the risk of an embolism.
Case Study (continued)
An IVC filter was subsequently inserted. Anticoagulation was initiated 7 days later, almost
2 weeks post SAH. An attempt was subsequently made to remove the IVC filter; however,
attempted retrieval of the IVC filter was unsuccessful because of the presence of a large
embolism which was trapped in the filter. The filter was therefore left in place. On
admission to rehabilitation he had been initiated onto anticoagulation, initially with heparin
and quickly switched over to Coumadin after the filter was put into place.
References
Amaragiri SV, Lees TA. Elastic compression stockings for prevention of deep vein thrombosis. Cochrane
Database Syst Rev 2000; CD001484.
Andre Ca, de Freitas GRa, Fukujima MMb. Prevention of deep venous thrombosis and pulmonary
embolism following stroke: a systematic review of published articles. European Journal of Neurology
2001; 14(1):21-32.
Eckman MH, Rosand J, Knudsen KA, Singer DE, Greenberg SM. Can patients be anticoagulated agter
intracerebral hemorrhage? A decision analysis. Stroke 2003; DOI:
10.1161/01.STR.0000078311.18928.16
Greenfield LJ, Michna BA. 12-year clinical-experience with the Greenfield vena-caval filter. Surgery
1988; 104(4):706-712.
- 60 -
Mazzone C, Chiodo Grandi F, Sandercock PAG, Miccio M, Salvi R. Physical methods for preventing
deep vein thrombosis in stroke. Coochrane Database of Systematic Reviews 2004 Issue 4. Art. No.:
CD001922. DOI: 10.1002/14651858.CD001922.pub2.
Muir KW, Watt A, Baxter G, Grosset DG, Lees KR. Randomized trial of graded compression stockings for
prevention of deep-vein thrombosis after acute stroke. QJM 2000; 93(6):359-64.
Prasad BK, Banerjee AK, Howard H. Incidence of deep vein thrombosis and the effect of pneumatic
compression of the calf in elderly hemiplegics. Age Aging 1982; 11:42-44.
Wasay M, Khan S, Zaki KS, Khealani BA, Kamal A, Azam I, Khatri IA. A non-randomized study of safety
and efficacy of heparin for DVT prophylaxis in intracerebral haemorrhage. J Pak Med Assoc. 2008;
58(7):362-364.
- 61 -
E8. Post-Stroke Seizure Disorders
- 62 -
E8. Post-Stroke Seizure Disorders
E8.1 Introduction and Case Study
Post stroke seizures may occur soon after stroke or be delayed; each appears to be associated
with differing pathogeneses. Most seizures are single, either partial or generalized (Ferro and
Pinto 2004. Wiebe and Butler (1998) noted that, “Seizures are the clinical expression of
excessive, hypersynchronous discharge of neurons in the cerebral cortex.”
Whether seizures worsen outcomes remains unclear. Vernino et al. (2003) reported new-onset
seizure among patients with ischemic stroke to be an independent risk factor for mortality on
multivariate analysis (Relative risk 1.81; 95%CI 1.16-2.83). Bladin et al. (2000) also reported
higher mortality among patients with seizures at 30 days and 1 year, compared to patients who
were seizure free (25% vs. 7% and 38% vs. 16%). However, the authors did not control for the
confounding effects of stroke severity or Comorbidity. The results of other studies have not
supported an increased risk of mortality (Labovitz et al. 2001, Reith et al. 1997).
Case Study
A 55-year old man is admitted into the inpatient rehabilitation unit 12 days post-stroke.
He had a cardioembolic stroke involving the territory of the left MCA, which is affecting
the cortex. He is consequently being treated with warfarin. During the second night in
the unit, the patient’s partner advised the nurse that he was making strong repetitive
movements with his right arm and thought he was having a seizure. When the nurse
arrived, the patient had a marked tendency to fall sleep and he felt very tired.
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Q1. What do you think caused this patient’s episode and what risk factors may have
contributed?
Answers
1. He likely suffered an epileptic seizure (the clinical expression of excessive, hypersyncronous
discharge of neurons in the cerebral cortex) (Wiebe and Butler 1998).
2. Younger patients and men are at increased risk for seizure activity post stroke (Arboix et al.
1997, Giroud et al. 1994). A lesion involving the cerebral cortex is a prerequisite for the
development of epilepsy (Olsen et al. 1987).
Q2. Would you describe this as epilepsy?
Answers
1. Epilepsy is a disorder of the brain characterized by an enduring predisposition to generate
epileptic seizures and by the neurobiologic, cognitive, psychological, and social
consequences of this condition. The definition of epilepsy requires the occurrence of at least
one seizure, although usually there needs to be more than one seizure.
2. One seizure in association with an enduring disturbance of the brain capable of giving rise to
other seizures has been defined as epilepsy (Fisher et al. 2005).
E8.2 Incidence of Post-Stroke Seizures
Q3. Discuss the incidence of seizures post-stroke.
Answers
1. The incidence of seizures following ischemic or hemorrhagic stroke in earlier series is noted
to be highly variable ranging from a low of 7.7% to a high of 42.8%. The average risk of
seizure post-stroke is 10% within 9-10 years after stroke.
2. Hemorrhagic stroke patients have been found to have an almost 2-fold risk of developing a
seizure following stroke compared to patients with an ischemic lesion (Bladin et al. 2000).
Discussion
Incidence of Post Stroke Seizures
Wiebe and Butler (1998) observed that the incidence of seizures following ischemic or
hemorrhagic stroke in earlier series is noted to be highly variable ranging from a low of 7.7% to
a high of 42.8%. This variability tends to be influenced by factors such study design, patient
population, diagnostic methods, and follow-up (Black 1983, DeRueck et al. 1980, Holmes 1980,
Louis and McDowell 1967, Meyer et al. 1971). Weibe and Butler suggest that high-resolution
imaging such as with computed tomography (CT) and magnetic resonance imaging (MRI) has
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improved the ability to identify and classify strokes, resulting in better estimates of their clinical
course and consequences.
In comparison to earlier studies, recent reports reveal less variability in the risk of post-stroke
seizures (PSS). The average risk of seizures is 10% within 9-10 years after stroke (Table
17.10), and well-conducted prospective studies report a 5-year cumulative incidence of 11.5%
(Burn et al. 1997). At least two studies suggest a higher incidence of PSS (15-17%) in patients
in rehabilitation units (Kotila and Waltimo 1992, Paolucci et al. 1997). It is not certain whether
this reflects seizure ascertainment bias (e.g., seizures are less likely to be missed in closely
observed patients), or a true increased seizure risk in this population (e.g., more extensive
cerebral injury) or both. Also, Cordonnier et al. (2005) reported that pre-existing dementia
increase the risk of late seizures defined as greater than one week post-stroke.
Black et al. (1983) reported 10% of all stroke patients developed seizures. Thirty-nine percent of
seizures occurred within the first 24 hours of stroke onset, 57% within the first week and 88%
within the first year. Sung and Chu (1986) demonstrated that for patients with intracerebral
hemorrhages, seizure onset time was very similar to that reported for other stroke entities; 30%
in the first 24 hours, 60% in the first two weeks and 90% in the first year. Sundaram and Chow
(1986) reported that in subarachnoid haemorrhage (SAH) patients, 84% of PSS took place
within the first 2 weeks of stroke onset.
The occurrence of post stroke seizures varies between 5% to 43%; or 10% on average.
Seizures usually occur during the first 1 to 2 weeks following stroke. Consequently, a majority
of seizure events will have already occurred before the patient is admitted to the stroke
rehabilitation unit.
Seizures Following Hemorrhagic Stroke
There is no consensus as to whether patients suffering from hemorrhagic strokes have a higher
incidence of seizures when compared to patients with infarctions. Some studies show evidence
to support this concept (Kilpatrick et al. 1990, Vespa et al. 2003), while others dispute the notion
that hemorrhagic strokes are associated with more PSS (Black et al. 1983, Olsen et al. 1987,
Shinton et al. 1988). Reith et al. (1997) found a higher frequency of early seizures (within 14
days of onset) in patients with intracerebral hemorrhages when compared to those with cerebral
infarction. However, in multivariate analysis, initial stroke severity was the sole predictor of
early PSS and the apparent increased frequency of PSS with intracerebral hemorrhage
reflected a higher initial stroke severity in this group of patients. Seizure incidence for
subarachnoid hemorrhagic patients has been found to be as high as 24% (Sundaram and Chow
1986).
Seizures in Cortical vs. Subcortical Strokes
The results of some studies showed that PSS only occurred in patients with cortical involvement
Lancman et al. 1993, Kilpatrick et al. 1990) while others did not (Gupta et al. 1988, Shinton et al.
1988). Olsen et al. (1987) found that a lesion involving the cerebral cortex, irrespective of size,
was a prerequisite for the development of epilepsy. Kilpatrick et al. (1990) supported this
concept by reporting an absence of seizure activity among 1,000 patients with subcortical
vascular strokes. For patients with hemorrhagic strokes, cortical involvement appeared to be
associated with the development of seizures, since deep-seated hemorrhages rarely cause
seizures (Kirkpatrick et al. 1990, Olsen et al. 1987, Sung and Chu 1986).
E8.3 Types and Timing of Post-Stroke Seizures
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Q4. What are the most common types of seizures after stroke and what is the relation
between seizures and time since the onset of stroke?
Answers
1. Black et al (1983) reported that 39% of seizures occurred within the first 24 hours, 57%
within the first week and 88% within the first year.
2. The overall percentage after stroke of focal seizures was 50%, generalized seizures 32%,
focal seizures with secondary generalization 15%, and complex partial seizures 2,5%.
(Wiebe-Velazquez and Blume 1993).
Discussion
Seizure Type Post Stroke
Wiebe-Velazquez and Blume (1993) totaled the frequency of various seizure types following
stroke from seven studies. From the combined 231 patients, the overall percentage of focal
seizures was 50%, generalized seizures 32%, focal seizures with secondary generalization 15%
and complex partial seizures 2.5%.
E8.4 Treatment of Post-Stroke Seizures
Q5. Describe traditional treatment approach to post-stroke seizures.
Answer
1. There is consensus opinion that post-stroke seizures should be treated with anticonvulsant
medication to prevent seizure recurrence.
2. Standard first-line therapy usually includes carbamazepine, valproic acid and phenytoin.
3. Phenytoin is known to interact with warfarin.
4. There is some concern that anti-epileptic drugs may impair recovery post stroke.
5. Benzodiazepines as an ongoing treatment should be avoided due to its sedating effects
unless seizure activity is uncontrolled.
Discussion
Treatment of Post- Stroke Seizures
There have been few studies of the treatment of seizures post stroke and no definitive evidence
recommending one treatment over another. There is consensus opinion that patients who have
experienced seizures post stroke should be given preventative anticonvulsant medication to
prevent seizure reoccurrence. Standard first-line therapy usually includes carbamazepine,
valproic acid and phenytoin sodium. However, phenytoin is known to interact with warfarin, a
commonly prescribed drug for patients who have suffered from a cardioembolic stroke. There is
some concern that the use of antiepilectic agents may impair recovery post stroke (Camilo &
Goldstein 2004), which should be a consideration in the decision of whether to treat an isolated
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seizure. The newer anti-epileptic drugs such as lamotrigine may be better tolerated and have a
better side-effect profile than some of the older drugs. Benzodiazepines as an ongoing
treatment should be avoided unless seizure activity is uncontrolled due to its sedating effects.
Current stroke guidelines from the Stroke Council of the American Heart Association and the
European Stroke Initiative also recognize the lack of evidence for treating stroke-related
seizures and defer to consensus level evidence: “Standard IV and oral antiepileptic drugs are in
general use…there is no evidence that prophylactic anticonvulsive treatment is beneficial…few
data concerning the efficacy of anticonvulsants in the treatment of stroke patients who have
experienced seizures…”(Adams et al. 2003, Broderick et al. 1999).
Only a single RCT has been conducted evaluating the efficacy of anticonvulsant therapy in
which one treatment was compared with another. Although the results were not statistically
significant the small sample size may have masked a real treatment effect of lamotrigine.
Lamotrigine may be a better treatment option compared with carbamazepine since lamotrigine
has relatively few side-effects, fewer potential drug interactions and does not require blood
monitoring in monotherapy. There is moderate evidence that lamotrigine is superior to
carbamazepine in the treatment of recurrent seizure post stroke.
E8.5 Treatment of Status Epilepticus Post Stroke
Q6. The nurse asks you how you would treat status epilepticus (just in case).
Answers
1. Benzodiazepines are considered the best first-line drugs for managing status acutely with a
seizure control rate of approximately 79%.
2. Both Lorazepam and Diazepan given intravenously are acute treatment strategies, although
Lorazepam may be more effective in terminating status epilepticus (59-89% VS 43-76%)
and has longer lasting anticonvulsivant properties (12 hours VS 20 Minutes for Diazepam).
3. Midazolam 10 mg given by the buccal and intranasal route is an alternative where
intravenous medications are difficult to give.
Discussion
Treatment of Status Epilepticus
On our stroke rehabilitation unit, benzodiazepines are considered the best first-line drugs for
managing status epilepticus acutely with a seizure control rate of approximately 79%. Both
lorazepam and diazepam given intravenously are equally acceptable acute treatment strategies,
although lorazepam may be more effective in terminating status epilepticus (59-89% vs. 4376%). Intravenous lorazepam is the preferred first line agent for seizure control due to its long
lasting anticonvulsant properties. Lorazepam lasts 12 hours versus 20 minutes for diazepam,
which places patients at risk of seizure recurrence unless a longer acting drug is given (A.
Bluvol, personal communication). The intravenous approach is invasive and is not always
preferred on the stroke rehabilitation unit. The newest benzodiazepine for seizure control is
midazolam, administered by several routes; intramuscular, intranasal and buccal. There is a
rapid onset of action (within five to 10 minutes), without accumulation or subsequent ‘hangover
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effect’. Metabolism is through a hepatic enzyme system with an elimination half-life of two
hours. Studies of midazolam in pediatric seizure patients have shown midazolam given by the
buccal or intranasal route is more, or as, effective as rectal diazepam and is the most reliably
absorbed i.m benzodiazepine for seizure treatment. On our own unit, 10 mg midazolam given
as 1 mL (5mg/mL) on each side of the mouth, between the teeth and inner aspect of the cheek,
is part of a medical directive and can be given by nursing staff. However, further research is
required to validate this treatment approach. A single RCT has examined the treatment of
seizures, specifically post stroke.
E8.6 Impact of Anti-Epileptic Medications on Stroke Recovery
Q7. The patient’s wife asks you if you need to treat the post-stroke seizures, that it
seems to slow him down, and she is worried about side effects. What would you advise
her?
Answers
1. There is some concern that the use of antiepileptic agents may impair recovery post stroke
(Camilo and Golgstein 2004).
2. Benzodiazepines as ongoing treatment should be avoided unless seizure activity in
uncontrolled due to its sedating effects.
3. There is consensus opinion that patients who have experienced seizures post stroke should
be given preventive anticonvulsant medication to prevent reoccurrence.
E8.7 Phenytoin as a Treatment of Post-Stroke Seizures
Q8. The medical student asks you about treating post-stroke seizures with
anticonvulsants. Is Phenytoin an appropriate treatment choice? What evidence is there
for anticonvulsants?
Answers
1. Phenytoin is known to interact with warfarin; indeed, phenytoin interacts with many other
drugs such us antibiotics.
2. There is no definitive evidence supporting one drug over another for the treatment of
epilepsy in post-stroke patients. Standard first-line therapy usually includes carbamazepine,
valproic acid, Lamotrigine and Phenytoin.
3. Gillad et al. (2007) showed that Lamotrigine may be better than Carbamazepine since
Lamotrigine has relatively few side-effects, fewer potential drug interactions, and does not
require blood monitoring in monotherapy.
E8.8 Driving and Post-Stroke Seizures
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Q9. The patient’s wife asks you about the possibility that her husband will be able to
drive again. What can you tell her about epilepsy and driving?
Answer
1. The patient should be assessed by a neurologist and an EEG performed.
2. There needs to be an assumption he has suffered a single seizure event.
3. He will need to be seizure-free for at least 6 months before he can drive again, presuming
the neurologist conducting the EEG concurs.
4. Individual circumstances may warrant prolonging or reducing the time period suggested.
Determining Medical Fitness to Operate Motor Vehicles: CMA Driver’s Guide 7th edition,
2006
10.4 Seizures
As for all conditions, in all instances where a temporal recommendation is made, the time
period should be considered a general guideline. Individual circumstances may warrant
prolonging or reducing the time period suggested.
10.4.1 Single, unprovoked seizure before a diagnosis
Private drivers: These patients should not drive for at least 3 months and not before a
complete neurologic evaluation — including electroencephalography (EEG) with waking and
sleep recording and appropriate neurologic imaging, prefereably magnetic resonance
imaging (MRI) — has been carried out to determine the cause.
Commercial drivers: Commercial drivers should be told to stop driving all classes of vehicles
at once. For these drivers, there is a need for even greater certainty that another seizure
will not occur while they are driving. As a minimum, commercial drivers should follow
the private driver guideline and not drive private vehicles for at least 3 months after a single,
unprovoked seizure. If a complete neurologic evaluation, including waking and sleep
EEG and appropriate neurologic imaging, preferably MRI, does not suggest a diagnosis
of epilepsy or some other condition that precludes driving, it is safe to recommend a
return to commercial driving after the patient has been seizure free for 12 months.
10.4.2 After a diagnosis of epilepsy
Patients may drive any class of vehicle if they have been seizure free for 5 years with or without
anticonvulsive medication.
Private drivers: Patients with epilepsy who are taking anti-seizure medication should not be
recommended for Class 5 or 6 licensing until the following conditions are met:
• Seizure-free period: The patient should be seizure free on medication for not less than 6
months, unless seizures with altered awareness have occurred more than once a year in
the previous 2 years, in which case the seizure-free interval should be 12 months. With certain
types of epilepsy, this period may be reduced to not less than 3 months on the
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recommendation of a neurologist, stating the reasons for this recommendation. The
seizure-free period is necessary to establish a drug level that prevents further seizures
without side effects that could affect the patient’s ability to drive safely. The anti-seizure
medication should have no evident effect on alertness or muscular coordination.
• Patient compliance with medication and instructions: The attending physician should feel
confident that the patient is conscientious and reliable and will continue to take the prescribed
anti-seizure medication as directed, carefully follow the physician’s instructions
and promptly report any further seizures. Medication compliance and dose appropriateness
should be documented with drug levels whenever reasonably possible.
Physicians should advise epileptic patients that they should not drive for long hours
without rest or when fatigued. Patients who require anti-seizure medication and who are
known to drink alcohol to excess should not drive until they have been alcohol and seizure
free for at least 6 months. These patients often neglect to take their medication while
drinking. As well, alcohol withdrawal is known to precipitate seizures and the use of even
moderate amounts of alcohol may lead to greater impairment in the presence of anti-seizure
medication. Patients taking these drugs should be advised not to consume more than 1 unit
of alcohol per 24 hours.
A patient who stops taking anti-seizure medication against medical advice should not be
recommended for driving. This prohibition on driving may change if the physician feels confident
that the formerly noncompliant patient, who is again taking anti-seizure medication as
prescribed, will conscientiously do so in the future and if compliance is corroborated by
therapeutic drug levels, when available.
Commercial drivers: It can be unsafe for commercial drivers who must take anti-seizure
medication to operate passenger-carrying or commercial transport vehicles (Classes 1–4).
For these drivers, there is a need for even greater certainty that another seizure will not
occur while they are driving. Commercial drivers are often unable to avoid driving for
long periods of time, frequently under extremely adverse conditions or in highly stressful
and fatiguing situations that could precipitate another seizure. Unfortunately, seizures do
sometimes recur even after many years of successful treatment.
Reference
Adams HP, Jr., Adams RJ, Brott T, et al. Guidelines for the early management of patients with ischemic
stroke: A scientific statement from the Stroke Council of the American Stroke Association. Stroke 2003;
34:1056-1083.
Arboix A, Garcia-Eroles L, Massons JB, Oliveres M, Comes E. Predictive factors of early seizures after
acute cerebrovascular disease. Stroke 1997; 28:1590-1594.
Black SE, Norris JW, Hachinski VC. Post-stroke seizures. Stroke 1983; 14:134, abstract.
Bladin CF, Alexandrov AV, Bellavance A, et al. Seizures after stroke: a prospective multicenter study.
Arch Neurol 2000; 57:1617-1622.
Broderick JP, Adams HP, Jr., Barsan W, et al. Guidelines for the management of spontaneous
intracerebral hemorrhage: A statement for healthcare professionals from a special writing group of the
Stroke Council, American Heart Association. Stroke 1999; 30:905-915.
- 70 -
Burn J, Dennis M, Bamford J, Sandercock P, Wade D, Warlow C 1997. Epileptic seizures after a first
stroke: the Oxfordshire Community Stroke Project. Br Med J 315:1582–1587.
Camilo O, Goldstein LB. Seizures and epilepsy after ischemic stroke. Stroke 2004; 35:1769-1775.
Cordonnier C, Henon, P Derambure P, Pasquier F, Leys D. Influence of pre-existing dementia on the risk
of post-stroke epileptic seizures. J Neurol Neurosurg Psychiatry 2005; 76:1649-1653.
De Reuck J, Krahel N, Sieben G, Orban L, de Coster W, vander Eecken H. Epilepsy in patients with
cerebral infarcts. Journal of Neurology 1980; 224(2):1432-1459.
Ferro JM, Pinto F. Poststroke epilepsy: epidemiology, pathophysiology and management. Drugs Aging
2004; 21:639-653.
Fisher RS, van Emde Boas W, Blume W, Elger C, Genton P, Lee P, Engel J Jr.Epileptic seizures and
epilepsy: definitions proposed by the International League Against Epilepsy (ILAE) and the International
Bureau for Epilepsy (IBE). Epilepsia. 2005; 46(4):470-2.
Gilad R, Sadeh M, Rapoport A, Dabby R, Boaz M, Lampl Y. Monotherapy of lamotrigine versus
carbamazepine in patients with poststroke seizure. Clin Neuropharmacol 2007; 30:189-195.
Giroud M, Gras P, Fayolle H, Andre N, Soichot P, Dumas R. Early seizures after acute stroke: a study of
1,640 cases. Epilepsia 1994; 35:959-964.
Gupta SR, Naheedy MH, Elias D. Post infarction seizures: A clinical study. Stroke 1988; 19:1477-81.
Holmes GL. The electroencephalogram as a predictor of seizures following cerebral infarction. Clinical
Electroencephalography 1980; 11(2):83-86.
Kilpatrick CJ, Davis SM, Tress BM. Epileptic seizures in acute stroke. Arch Neurol 1990; 47:157-60.
Kotila M, Waltimo O. Epilepsy after stroke. Epilepsia 1992; 33:495-498.
Labovitz DL, Hauser WA, Sacco RL. Prevalence and predictors of early seizures and status epilexticus
after first stroke. Neurology 2001; 57:200-206.
Lancman ME, Golimstock A, Norscimi J, Granillo R. Risk factors for developing seizures after stroke.
Epilepsia 1993; 34:141-143.
Louis S, McDowell F. Epileptic seizures in nonembolic cerebral infarction. Archives of Neurology 1967;
17(4):414.
Meyer JS, Charney JZ, Rivera VM, Mathew NT. Cerebral embolization: prospective clinical analysis of 42
cases. Stroke 1971; 2:541-554.
Olsen TS, Hogenhave H, Thage O. Epilepsy after stroke. Neurology 1987; 37:1209-11.
Paolucci S, Silverstri G, Lubich S, Pratesi L, Traballesi M, Gigli GL. Post stroke late seizures and their
role in rehabilitation of inpatients. Epilepsia 1997; 38(3):266-270.
Reith J, Jorgensen HS, Nakayama H, Raaschou HO, Olsen TS. Seizures in acute stroke: predictors and
prognostic significance. The Copenhagen Stroke Study. Stroke 1997; 28:1585-1589.
Shinton RA, Gill JS, Melnick SC. The frequency, characteristics and prognosis of epileptic seizures at the
onset of stroke. J Neurol Neurosurg Psychiatry 1988; 51:273-76.
- 71 -
Sundaram MBM, Chow F. Seizures associated with spontaneous subarachnoid hemorrhage. Can J
Neurol Sci 1986; 13:229-31.
Sung CY, Chu NS. Epileptic seizures in intracerebral hemorrhage. J Neurol Neurosurg Psychiatry 1986;
52:1273-76.
Vernino S, Brown RD, Jr., Sejvar JJ, Sicks JD, Petty GW, O'Fallon WM. Cause-specific
mortality after first cerebral infarction: a population-based study. Stroke 2003; 34(8):1828-1832.
Vespa PM, O'Phelan K, Shah M et al. Acute seizures after intracerebral hemorrhage: a factor in
progressive midline shift and outcome. Neurology. 2003; 60:1441-1446.
Wiebe S, Butler JT 1998. Poststroke seizures and epilepsy. In: Teasell R (editor): Physical Medicine and
Rehabilitation: State of the Art Reviews. Philadelphia: Hanley and Belfus. pp. 405–422.
Wiebe-Velazquez S, Blume WT. Seizures. In: Teasell RW (ed). Physical Medicine and Rehabilitation:
State of the Art Reviews. Long-Term Consequences of Stroke. Philadelphia, Hanley & Belfus, 1993;
7(1):73-87.
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E9. Central Pain State
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E9. Central Pain State
E9.1 The Incidence of Central Pain Post Stroke
Q1. What is the incidence of central pain post stroke?
Answer
1. Central post-stroke pain occurs in less than 2% of stroke patients.
Discussion
Central Post Stroke Pain (CPSP) is generally regarded as rare, occurring in less than 2% of
strokes (Pagni 1984, Mucke and Miaciewicz 1987, Tasker 1990), although a recent study
reported an 8% incidence among unselected stroke patients with 5% reporting moderate to
severe pain (Andersen et al. 1995). Determining the actual incidence of CPSP is difficult since
most studies have been based on selected cases (Hansson 2004). A prolonged gap between
the stroke event and the onset of pain may also hinder a diagnosis.
E9.2 Pathophysiology of Central Pain Post Stroke
Q2. What is the pathophysiology of central pain post stroke?
Answers
1. The pathophysiology of central pain post stroke remains largely unknown.
2. Must be damage to the spino-thalamo-cortical pathway with disturbance in temperature and
pain sensation.
3. Damage to the spinothalamiocortical tract resulting in denervation hyperexcitability of
cortical or thalamic neurons are currently the most popular hypothesis for the pain.
4. Spontaneous or evoked dysesthesia, allodynia/hyperalgesia are manifestations of central
post-stroke pain; paradoxical allodynia with associated numbness in the same territory.
Discussion
Central pain resulting from a stroke is often referred to as "thalamic pain" despite the fact that in
many patients with CPSP, the cerebrovascular lesions do not involve the thalamus (Leijon et al.
1989a, Fields and Adams 1974, Loh et al. 1981, Agnew et al. 1983, Bowsher and Laheuerta
1985, Garcin and Lapresle 1969). Leijon et al. (1989a) noted that central pain states occurred
following lower brainstem, thalamic and suprathalamic cerebrovascular events. CPSP is
invariably associated with a lesion involving the spino-thalamo-cortical pathway with a
disturbance in temperature and pain sensation (Andersen et al. 1995).
At present, the pathophysiology of CPSP states remains unknown. It is becoming increasingly
clear that damage to the spinothalamicocortical pathway is associated with CPSP (Bovie et al.
1989, Jensen and Lenz 1995, Andersen et al. 1995, Vestergaard 1995, Dejerine and Roussy
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1906) although not all patients with damage to this pathway experience pain (Andersen et al.
1995). CPSP is always associated with impaired sensory perceptions to cold and warm stimuli
and to pinprick; these somatosensory functions are mediated by the spinothalamic tract (Bovie
et al. 1989, Boivie 1992, Vestergaard et al. 1995). However, touch, 2-point discrimination and
vibration sense, generally regarded to be mediated by lemniscal pathways in the CNS and often
involved in CPSP states, may be intact (Boivie et al. 1989, Vestergaard et al. 1995).
Vestergaard et al. (1995) reported that lemniscal system lesions are not necessary for the
development of CPSP.
Most, but not all cases of CPSP, are associated with hyperalgesia and/or allodynia. This
paradoxical presence of a sensory deficit in combination with hyperalgesia in that part of the
body de-afferented by the stroke lesion suggests a central sensitization of third and fourth order
CNS neurons as a result of loss of spino-thalamic (or thalamo-cortical) input (Vestergaard et al.
1995). Hyperexcitability of thalamic or cortical neurons could evoke the perception of pain.
Vestergaard et al. (1995) noted that this hypothesis shares many features thought to be
characteristic of other neuropathic pain syndromes associated with peripheral nerve lesions
where spinal cord neurons that have lost their afferent input develop a central hyperexcitability
(Bennett and Laird 1992, Dubner 1991, Wall 1991).
Conclusions Regarding the Pathophysiology of Post-Stroke Central Pain
Damage to the spinothalamiocortical tract appears to be necessary with denervation
hyperexcitability of cortical or thalamic neurons being the most popular hypothesis for the pain.
Spontaneous or evoked dysesthesia, allodynia/hyperalgesia are manifestations of central poststroke pain.
Case Study
A 46 year old male sustained a right subcortical hemorrhage. He subsequently
experienced gradual improvement in his motor function so that he was again ambulatory
without support. However, since about one month after his stroke he had been troubled
by a painful “pins and needles” sensation involving his entire left side, except for his scalp.
He also had a burning pain (“like a sunburn”) without superimposed shooting or lancinating
pains. He was more comfortable at rest with a reported pain intensity of about 4/10. He
had extreme sensitivity to light touch and other stimulation involving the left side of his
body and in particular, just rubbing of his clothes while walking exacerbated his pain
significantly. On neurological examination his cranial nerves were intact, motor tone was
normal although there was a left sided pronator drift and mild weakness in left hip flexion.
Fine finger coordination was normal bilaterally. On sensory examination there was blunting
to pinprick involving his entire left side, except for his face. He had marked touch evoked
pain or allodynia on the left side. The cold tuning fork was perceived as being even colder
on the left side. Vibration sense was impaired in the left fingers and toes and he had
difficulty detecting fine excursion of the left toes. Cortical sensation was intact and in
particular, there was no sensory neglect. Gait testing revealed less arm swing on the left
which was directly related to the fact that stimulation from his clothes increased his pain.
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E9.3 Defining Post-Stroke Central Pain States
Q3. Define and Describe the Post-Stroke Central Pain State.
Answer
1. Central pain is pain due as a direct consequence of the stroke.
2. Described as burning or unpleasant sensations (parasthesiae) made worse with physical
movements, emotional stress, cold, and light touch.
3. Associated sensory abnormality on affected side.
Discussion
Central pain is often described as a “burning” sensation in association with an unpleasant
association of tingling, pins and needles, or numbness (Tasker 1990). It is often described in
terms such as ripping, tearing, pressing, twisting, aching, pricking, and lacerating (Boivie et al.
1989, Leijon et al. 1989a, Anderson et al. 1995, Tasker 1990). The pain is generally constant
and often associated with spontaneous paroxysms of pain (Boivie et al. 1989, Leijon et al.
1989a, Tasker 1990, Frese et al. 2006). It can also be exacerbated by physical movements,
emotional stress, loud noises or voices, changes in the weather, cold and light touch (Boivie et
al. 1989, Leijon et al. 1989a, Tasker 1990). All patients with CPSP generally have some kind of
sensory abnormality on the affected side (Boivie et al. 1989). Decreased pinprick and threshold
abnormalities to temperature detection are invariably present with touch, vibration, and twopoint discrimination being more variably involved. Virtually all patient report spontaneous or
evoked parasthesias and/or dysaesthesia (Leijon et al. 1989a, Andersen et al. 1995).
Spontaneous dysesthesias occur in the majority of CPSP patients while almost all demonstrate
some hypersensitivity to an external somatic stimuli (Leijon et al. 1989a). Hence the
spontaneous pain seen in central pain states may be accompanied by further unpleasant effects
induced by somatosensory stimuli known as hyperalgesia, allodynia and dysesthesia.
Q4. Define the terms “dysesthesia”, “allodynia”, and “hyperalgesia”.
Answers
1. Dysesthesia: Unpleasant sensations, either spontaneous or evoked (Andersen et al. 1995).
2. Allodynia: Abnormally unpleasant somatosensory experience, often poorly localized,
elucidated by normally non-nociceptive stimuli (Andersen et al. 1995).
3. Hyperalgesia: Increased pain response to a normally painful stimulus (Andersen et al.
1995).
E9.4 Treatment of Central Post-Stroke Pain
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Q5. Describe an algorithm treatment approach to Central Post Stroke Pain.
Answer
1. Majority of CPSP are intractable to therapeutic interventions.
2. First line treatments include tricyclic antidepressants and antiepileptics.
3. Second line treatment is opioids.
Discussion
The majority of central post stroke pain states are intractable to therapeutic interventions. A
number of interventions are commonly seen, the interventions which are the most likely to have
a benefit are pharmacological interventions. Moreover, Henry et al. (2008) have noted, “Our
incomplete understanding of the mechanism underlying CPSP challenges the development of
targeted treatment strategies (Hansson 2004). Moreover, the dearth of published data from
large, well-designed clinical trials involving patients with CPSP has created a situation where
guidelines for treatment are based upon “uncontrolled studies, clinical experience and expert
opinion” (Gordon 2007).” (Henry et al. 2008). Unfortunately, the medical literature does not
provide us with anything more than consensus and anecdotal experience as to the best
approach to treat CPSP.
Algorithm for Treatment of CPSP (Gordon 2007)
First-line treatment: Tricyclic antidepressants such as amitriptyline and nortriptyline as well as
antiepileptics such as lamotrigine, gabapentin, pregabalin and carbamazepine.
Second-line treatment: Opioids such as morphine or levorphanol may be prescribed.
Not Recommended: Nonsteroidal anti-inflammatory drugs are not recommended. Local
anaesthetics such as lidocaine, N-methyl-D-aspartate receptor antagonists including ketamine,
cannabinoids, and botulinum toxin A are not recommended.
First-Line Treatments
First-line treatment should be tricyclic antidepressants such as amitriptyline and nortriptyline as
well as antiepileptics such as lamotrigine, gabapentin, pregabalin and carbamazepine.
Amitriptyline: It has been noted that Amitriptyline, a tricyclic antidepressant, is usually the drug
of first choice (Bowsher 1999, Leijon and Boivie 1989, Lampl et al. 2002). Based on the results
of two RCTs, the SREBR (11th edition 2008) notes that there is conflicting evidence that
treatment of amitriptyline results in a reduction of pain post stroke (Teasell et al. 2008). Henry
et al. (2008) have noted that, “its utility is limited by common adverse effect ts such as dry
mouth, drowsiness and constipation, as well as more rare instances of urinary retention,
orthostatic hypotension and cardiac arrhythmia (Hansson 2004). … the dose and blood levels of
amitriptyline associated with pain relief are in the lower range of doses required for resolution of
depression (McQuay et al. 1993).”
Anti-Epileptic Treatments: There is moderate evidence that Lamotrigine may be an
alternative to tricyclic antidepressants in the treatment of central post stroke pain.
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SSRI Antidepressants: There is limited evidence that selective serotonin reuptake inhibitor
fluxoxamine treatment is useful for the treatment of CPSP relatively early after a stroke.
Second-Line Treatments
For patients refractory to first-line treatment, opioids such as morphine or levorphanol may be
prescribed.
Opioids: There is moderate evidence, based on one RCT, that intravenous morphine induced
analgesic effects on some components of central neuropathic pain syndromes, but only a
minority of patients may benefit from long-term opioid treatment. There is moderate evidence
that high-strength u-opioid agonist levorphanol is effective in reducing pain in post-stroke
patients.
Not Recommended Treatments
Nonsteroidal anti-inflammatory drugs are not recommended. Local anaesthetics such as
lidocaine, N-methyl-D-aspartate receptor antagonists including ketamine, cannabinoids, and
botulinum toxin A are also not recommended
Intravenous Lidocaine
Based on the results from a single RCT, there is moderate evidence that intravenous lidocaine
results in short-term pain relief; however, the results are not maintained at 6 hours following
treatment.
Non- Pharmacological Treatments
Nonpharmacological treatments of central post stroke pain are considered more adjuncts to
treatment.
Motor Cortex Stimulation
There is limited evidence that motor cortex stimulation can provide long-term pain relief.
Case Study (continued)
When seen almost 18 months later, he had been tried on tricyclic antidepressants without
benefit. He continued on Tegretol 100 mg BID which was the maximum dose he was able
to tolerate, He also took Tylenol #2 x2 tablets up to 4 times daily with minimal relief. He
was Lorazepam one tablet at night.
Q6. What options would be available now?
Answer
1. Second-line treatment would include stronger narcotic analgesics such as Oxycodone
(short-acting or long-acting) or Morphine (long-acting).
2. Alternative anti-epileptics such as Dilantin, Gabapentin and Pregablin.
- 78 -
Case Study (continued)
The patient was initiated on a stronger analgesic Percocet 2 tablets qid and Neurontin
(Gabapentin), gradually increasing dose to 300 mgs qid as well as Venlafaxine 75 mg daily.
Duragesic was initiated and increased to 50 mcg per hour but was only receiving pain relief
for the first 2 of 3 days. He experienced moderate but still inadequate pain relief. His
Neurontin was increased to 1,600 mg tid without pain relief and Dilantin 350 mg daily was
added to deal with seizures. Duragesic was increased to 150 mcg per hour every 2 days.
Methadone was used to replace the Duragesic at a rate of 20 mg tid whch was increased
to 50 mg q6h. Neurontin was decreased and Lyrica initiated at 300 mg bid; Venlafaxine
was increased to 150 mg daily while Nabilone was given at 1mg daily.
References
Agnew DS, Shetter AG, Segall HD, Flom RA. Thalamic pain. In Bonica J, Lindblom U, Iggo A (eds).
Advances in Pain Research and Therapy Vol. 5, Raven Press, New York, 1983, p. 941-946.
Andersen G, Vestergaard K, Ingeman-Nielsen M, Jensen TS. Incidence of central poststroke pain. Pain
1995; 61:187-193.
Bennett GJ, Laird JMA. Central changes contributing to neuropathic hyperalgesia. In: Willis WD (ed),
Hyperalgesia and Allodynia, Raven Press, New York, 1992, pp. 305-310.
Boivie J. Hyperalgesia and allodynia in patients with CNS lesions. In W.D. Willis Jr. (ed.), Hyperalgesia
and Allodynia, Raven Press, New York, 1992, pp. 363-373.
Boivie J, Leijon G, Johansson I. Cental poststroke pain - a study of the mechanisms through analyses of
the sensory abnormalities. Pain 1989;37:173-185 (a).
Bowsher D, Laheuerta J. Central pain in 22 patients: clinical features, somatosensory
changes and CT scan findings. J Neurol 1985; 232:237-297.
Dejerine J, Roussy G. La syndrome thalamique. Rev Neurol 1906; 14:521-532 (also see
Wilkins RH, Brody IA. The thalamic syndrome. Arch Neurol 1969; 20:55).
Dubner R. Neuronal plasticity and pain following peripheral tissue inflammation or nerve injury. In: Bond
MR, Charlton JE, Woolf CJ (eds). Pain Research and Clinical Management, Vol. 4, Proc. VIth World
Congress on Pain, Elsevier, Amsterdam, 1991, pp.263-276.
Fields HL, Adams JE. Pain after cortical injury relieved by electrical stimulation of the internal capsule.
Brain 1974; 97:169-178.
Frese A, Husstedt IW, Ringelstein EB, Evers S. Pharmacologic Treatment of Central Post-Stroke Pain.
Clin J Pain 2006; 22(3):252-260.
Garcin R, Lapresle J. Incoordination cerebrelleuse du membre inferieur par lesion localiseu dans la
region intern du thalamus control-lateral. Rev Neurol (Paris) 1969; 120:5.
- 79 -
Gordon A. Best practive guidelines for treatment of central pain after stroke. In: Henry JL, Panju A,
Yashpal K, eds. Central Neuropathic Pain: Focus on Poststroke Pain. Seattle: IASP Press, 2007.
Hansson P. Post-stroke pain case study: Clinical characteristics, therapeutic options and long-term
follow-up. Eur J Neurol 2004; 11(Suppl 1):22-30.
Jensen TS, Lenz FA. Central post-stroke pain: a challenge for the scientist and the clinician. Pain 1995;
61:161-164.
Lampl C, Yazdi K, Roper C. Amitriptyline in the prophylazis of central poststroke pain. Preliminary
results of 39 patients in a placebo-controlled, long-term study. Stroke 2002; 33:3030-2.
Leijon G, Boivie J, Johansson I. Central poststroke pain - neurological symptoms and pain
characteristics. Pain 1989; 36:13-25(a).
Leijon G, Boivie J. Central post-stroke pain – a controlled trail of amitriptyline and carbamazepine. Pain
1989; 36:27-36.
Loh L, Nathan PW, Schott GD. Pain due to lesions of central nervous system removed by sympathetic
block. Br Med J 1981; 282:1026-1028.
McQuay HJ, Carroll D, Glynn CJ. Dose-response for analgesic effect of amitriptyline in chronic pain.
Anaeathesia 1993; 106:3-8.
Mucke L, Maciewicz R. Clinical management of neuropathic pain. Neurol Clin 1987; 5(4):649-662.
Pagni CA. Central pain due to spinal cord and brainstem damage. In Wall PD, Melzack R
(eds). Textbook of Pain, Churchill Livingstone, London, 1984, p. 481-495.
Tasker RR. Pain resulting from central nervous system pathology (central pain). In Bonica JJ (ed). The
Management of Pain, Lea & Febiger, Malvern, PA, Vol 1, 2nd ed, 1990, p 264-283.
Teasell RW, Foley NC, Salter K, Bhogal SK, Jutai J, Speechley MR. Evidence-Based Review of Stroke
Rehabilitation (11th edition). Canadian Stroke Network; 2008.
Vestergaard K, Nielsen J, Andersen G, Ingeman-Nielsen M, Arendt-Nielsen L, Jensen TS. Sensory
abnormalities in consecutive, unselected patients with central post-stroke pain. Pain 1995; 61:177-185.
Wall PD. Neuropathic pain and injured nerve: central mechanisms. Br Med Bull 1991; 47:631-643.
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E10. Urinary Incontinence
- 81 -
E10. Urinary Incontinence
Canadian Stroke Strategy Guidelines: Recommendation 4.2d – Continence
i. All stroke patients should be screened for urinary incontinence and retention (with or without
overflow), fecal incontinence and constipation [Evidence Level C] (RNAO).
ii. Stroke patients with urinary incontinence should be assessed by trained personnel using a
structured functional assessment [Evidence Level B] (AU).
iii. The use of indwelling catheters should be avoided. If used, indwelling catheters should be
assessed daily and removed as soon as possible [Evidence Level C] (AU, CSQCS, RCP,
VA/DoD).
iv. A bladder training program should be implemented in patients who are incontinent of urine
[Evidence Level C] (AU, VA/DoD).
v. The use of portable ultrasound is recommended as the preferred noninvasive painless
method for assessing post-void residual and eliminates the risk of introducing urinary infection or
causing urethral trauma by catheterization [Evidence Level C] (CCF).
E10.1 Normal Bladder Functioning
Q1. Describe the various areas of the central nervous system and peripheral nervous
systems involved in the storage and emptying of urine.
Answer
Normal Bladder (detrusor) and urethral functioning involves the following areas of the central
and peripheral nervous systems (Borrie1998):
1. The sympathetic nervous system relaxes the detrusor muscle while internal urethral
sphincter control is maintained by sympathetic alphaadrenoreceptors.
2. Parasympathetic acetylcholine receptors mediate detrusor contracture.
3. Somatic (voluntary) nervous system innervates the pelvic floor muscles, including the
external urethral sphincter.
4. A micturition centre in the brainstem (pons) informs when the bladder is filling and controls
the sacral reflex when bladder filling reaches a certain level.
5. The micturition centre in the frontal lobes provides conscious input to the pontine micturition
centre allowing the inhibition of urination until the time of voluntary control.
Discussion
Normal Bladder Function
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Bladder (detrusor) and urethral functions are coordinated for the storage and emptying of urine
(Borrie 1998). This involves areas of the central nervous system and multiple peripheral nervous
systems as listed below:
1. Sympathetic nervous system relaxes the detrusor muscle while internal urethral sphincter
control is maintained by sympathetic alpha-adrenoreceptors
2. Parasympathetic acetylcholine receptors mediate detrusor contracture.
3. Somatic (voluntary) nervous system innervates the pelvic floor muscles, including the
external urethral sphincter.
4. A micturition centre in the brainstem (pons) inform when the bladder is filling and controls
the sacral reflex when bladder filling reaches a certain level.
5. The micturition centre in the frontal lobes provides conscious input to the pontine micturition
centre allowing the inhibition of urination until the time of voluntary control.
Normally, we are unaware of bladder fullness until a capacity of about 300 cc is reached. The
need to void is then inhibited or controlled by the frontal lobes.
E10.2 Urinary Dysfunction Post Stroke
Q2. Describe the different types of urinary dysfunction occur post-stroke.
Answer
1. The most frequently occurring voiding abnormalities associated with a stroke have been
identified as urinary frequency, urge incontinence and urinary retention (Marinkovic and
Badlani 2001).
2. Urinary tract infection is not uncommon in stroke patients.
Discussion
Urinary Incontinence (UI) is defined as any involuntary leakage of urine (Abrams et al. 2002).
Commonly seen post-stoke, UI is a strong predictor of poor functional recovery, discharge to
long-term care, and limited resumption of social participation (Dumoulin et al. 2007).
Urinary Retention is commonly reported post acute stroke but less commonly seen in the
rehabilitation phase. Stroke itself can cause retention but other contributing factors may include
an inability to communicate the need to void, decreased level of consciousness or restricted
mobility.
Q3. What three mechanisms are thought to be responsible for urinary incontinence post
stroke?
Answers
1. Detrusor hyperreflexia. Urge incontinence and bladder hyperreflexia from damage to
neuromicturition pathways.
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2. Bladder retention. Overflow incontinence related to diabetic neuropathy or medications.
3. Stroke related barriers: paresis, cognition and language deficits.
Discussion
Gelber et al. (1993) suggested that three mechanisms were responsible for incontinence post
stroke (van Kuijk et al. 2001). These included:
 Most common problems is detrusor hyperreflexia with urge incontinence and bladder
hyperreflexia from disrupted neuromicturition pathways (frontal lobe or pontine micturition
centers) (Nazarko 2003, Fader & Craggs 2003).
 Incomplete bladder emptying with overflow incontinence and bladder hyporeflexia from
concurrent neuropathy or from the concurrent medications, such as diuretics (Fader &
Craggs 2003).
 Incontinence from stroke-related motor, cognitive and language deficits, despite normal
bladder function.
Subtypes of Urinary Incontinence
Type
Signs & Symptoms
Urge
Strong, sudden need
to void.
Stress
Mixed
Overflow
Urodynamic Findings
Cystometry shows
evidence of leakage
with detrusor
contractions only.
Loss associated with Leakage during
effort or exertion
cystometry filling,
(such as sneezing,
without detrusor
jumping, or laughing). contractions.
Urge to void
Leakage during
combined with loss
cystometry filling, with
on effort or exertion.
and without detrusor
contractions.
Frequent small voids Postvoid residual
/ loss with movement. (PVR) urine >150 ml.
Pathophysiology
Detrusor instability.
Sphincter
incompetence.
Sphinter
incompetence
combined with
detrusor instability.
Outlet obstruction
and/or poorly
contractile detusor.
Functional or Cognitive, language,
Iatrogenic
and/or mobility
deficits or the use of
anticholinergic
medications.
E10.3 Detrusor Hyperreflexia Post Stroke
Q4. Discuss detrusor hyperreflexia.
Answer
Hyperactive bladder empties suddenly at a usually lower than normal volume.
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Discussion
Cortical and subcortical strokes generally result in an unstable or hyperreactive detrusor (Borrie
1998). Borrie (1998) has noted that unstable detrusor contractions occur with little warning and
result in symptoms of urinary urge incontinence. The bladder volume at which this occurs can
be variable but it is usually lower than the volume at which a person with a normally functioning
bladder would normally have a strong urge to void (Borrie 1998). Borrie (1998) notes that
detruson hyperreflexia is not inevitable following a stroke. It has been noted that urinary
incontinence is more common with larger strokes with a greater number of accompanying
deficits and is closely associated with bowel incontinence, dysphagia and overall functional
level, all markers of more severe strokes.
E10.4 Urinary Retention Post Stroke
Q5. Discuss urinary retention and potential contributing factors.
Answer
1. Urinary retention is common following an acute stroke (21-47%).
2. Potential contributing factors include difficulty with communication, mobility and decreased
consciousness.
3. Other contributing factors may be a hypreflexic bladder, as seen in diabetic neuropathy, or
an obstruction such as prostatic hypertrophy.
4. Occasionally urinary retention will persist in very severe stroke patients, often in patients
with embolic strokes with no previous warnings.
Discussion
Urinary retention is commonly reported acutely following stroke; percentages of 21-47% post
stroke have been reported (Doshi et al. 2003, Burney et al. 1996). Although stroke itself can
cause retention, consequences of stroke including an inability to communicate the need to void,
decreased level of consciousness, or restricted mobility may also be contributory (Marinkovic
and Badlani 2001). Anecdotally, urinary retention is sometimes seen in the rehabilitation phase
of stroke care, often in more severe stroke patients, although surprisingly little has been written
on the subject. Retention may also be associated with prostatic hypertrophy in males, although
usually there is a history of some difficulty prior to the stroke. Urinary retention can also be
seen in patient with severe neuropathies, diabetics are the most common, with a hyporeflexic
bladder. Incomplete bladder emptying with significant residual urine is a significant risk factor
for the development of urinary tract infections.
E10.5 Other Factors Contribuing to Post-Stroke Incontinence
Q6. Discuss Other Factors Contributing to Post-Stroke Incontinence.
Answers
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Stroke results in a number of factors which can affect continence, but which are often
overlooked:
1. Communication difficulties, particularly an inability to communicate voiding needs, either due
to aphasia, dysarthria or confusion/cognitive impairments.
2. Mobility problems, such as hemiplegia make some patients dependent on caregivers to void
in a socially appropriate manner. Lack of caregiver support may also make it difficult to toilet
the stroke patients quickly enough.
3. Post stroke depression and confusion may result in a failure to communicate the need for
assistance.
4. Medications, such as diuretics can increase the frequency of the need to void; others can
increase confusion, while still others such as antihypertensives may affect the autonomic
nervous system leading to retention.
Discussion
Nazarko (2003) notes that it has been suggested that continence problems post stroke are a
common consequence of immobility and dependency as opposed to neurological loss of control
(Fader and Craggs 2003).
E10.6 Course of Urinary Incontinence Post Stroke
Q7. How common is urinary incontinence following stroke? What is the natural history?
Answer
1. Urinary incontinence has been reported in 37-79% of stroke patients in the acute phase and
17% of stroke survivors in the community.
2. Most incontinence resolves without treatment over 8 weeks although a significant
percentage (14-19%) still have incontinence at 6 months.
Discussion
Brooks (2004) has noted that a stroke may exacerbate existing stress incontinence, a problem
more common in women. Urinary incontinence is a common problem following a stroke with
reported incidences ranging from 37% to 79% (van Kuijk et al. 2001, Forster and Young 2002,
Brittain et al. 1985). The discrepancies in the reported rates likely arise from differing definitions
of incontinence used and the populations under study. Urinary incontinence was reported
among 17% (n=213) of non-institutionalized post stroke survivors, an average of nine years post
stroke, compared to 7% of control subjects without stroke (Jorgensen et al. 2005) (OR=2.8,
95% CI; 1.5-5.2). Incontinence post stroke often resolves without treatment in eight weeks
(Borrie et al. 1986, Brocklehurst et al. 1985). Borrie (1998) has noted that “44-60% of stroke
victims have urinary incontinence (Borrie et al. 1986, Brocklehurst et al. 1985, Nakayama et al.
1997) and of these, 17-22% will have premorbid urinary incontinence (Benbow et al. 1991,
Borrie et al. 1986). 14-19% have persisting incontinence (Barer 1989, Nakayama et al. 1997) at
six months.”
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E10. 7 Risk Factors for Urinary Incontinence Post Stroke
Q8. What are the risk factors for urinary incontinence post stroke?
Answers
1. Severe strokes have a higher incidence of urinary incontinence.
2. Premorbid history of urinary incontinence, i.e comorbidities.
3. Motor weakness and mobility difficulties, including ataxia.
4. Altered level of consciousness.
5. Cognitive impairment
6. Depression
7. Elderly
8. Diabetic
Discussion
Patients who experience severe strokes are those that tend to have the greatest difficulty with
incontinence (Nazarko 2003). Brittain et al. (1999) noted that non-neurological factors such as
pre-morbid incontinence or stroke-related impairments, such as motor weakness, altered level
of consciousness, cognitive impairment, ataxia and sensory lesions, in the presence of
otherwise normal bladder function can contribute to the increase in incontinence. Normal agerelated changes in bladder function may also independently affect recovery (Marinkovic and
Badlani 2001). Jorgensen et al. (2005) identified depression, motor leg function and cognitive
impairment as risk factors for incontinence. Gariballa (2003) found that patients with urinary
incontinence at admission tended to be more undernourished and dehydrated, more impaired,
at greater risk for infective complications and older then patients without urinary incontinence. A
study of 935 acute stroke patients demonstrated that significant risk factors for post stroke
urinary incontinence included age, severity of stroke, diabetes and comorbidity associated with
other pre-existing disabling diseases (Nakayama et al. 1997).
E10.8 Consequences of Urinary Incontinence Post Stroke
Q9. Discuss the relationship between urinary incontinence and institutionalization.
Answers
Stroke survivors with persistent urinary incontinence tend to have greater disability, a poor
prognosis, greater morbidity and mortality during their hospital stay and are more likely to be
institutionalized.
Discussion
Brocklehurst et al. (1985) noted that while problems with bladder control and incontinence are
common after stroke, they tend to resolve spontaneously in the majority of stroke patients.
Recovery from post-stroke urinary incontinence is associated with less disability and lower rates
of institutionalization than persistent incontinence (Patel et al. 2001). Bean et al. (2003) noted
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an almost 2-fold difference in level of disability post-stroke among those who were incontinent
versus those were continent (p<0.001). One study found that patients suffering from urinary
incontinence on admission often had greater morbidity and mortality throughout their hospital
stay and at 3 months post-stroke (Gariballa 2003). As noted by several investigators
(Jongbloed 1986, Reding et al. 1987, Jawad and Ward 1999), recurring incontinence denotes a
long-term poor prognosis for functional recovery. As Forster and Young (2002) note, “treatment
evidence specific to stroke is limited.”
Brittain et al. (2000) reported that a significant higher proportion of community-dwelling persons
who had experienced a stroke had more urinary symptoms compared to those that had never
had a stroke (64% vs. 33%). The difference was statistically significant even after adjusting for
age and sex differences between the groups. Stroke survivors were 1.77 times more likely to
experience urinary symptoms than non-stroke persons. More stroke survivors reported a
significant impact on lifestyle than did the non-stroke subjects. Twice as many stroke survivors
than non-stroke persons reported that their urinary symptoms were moderate to severe.
Kolominsky-Rabas et al. (2003) examined the occurrence of urinary incontinence (UI) and the
long-term effect UI had on subjects’ prognosis and institutional status following stroke within a
community-based population. Throughout the acute phase 41% of patients had full UI, 12% had
partial UI and 47% had no UI (16%, 16% and 68% respectively at 12-months follow-up). In
total, patients’ institutionalized at 12-months follow-up included 45% of patients with UI
compared to only 5% of patients without UI. The authors concluded that the risk of
institutionalization 1-year post stroke is a “fourfold higher” for stroke patients with UI in the acute
phase of rehabilitation.
E10.9 Urinary Tract Infection Post Stroke
Q10. How common are UTIs Post Stroke and what are risk factors for UTI?
Answers
1. UTI is the most common medical complication in stroke rehabilitation.
2. Risk factors include use of beta-blockers and high post-void residuals.
Discussion
Urinary tract infections (UTI) are the most commonly encountered medical complication
associated with stroke rehabilitation (Roth et al. 2001). Although age greater than 65, male sex,
a history of prior stroke, stroke syndrome, use of β-Block or antidepressants and a post void
residual (PVR) of 150 mL or more have been reported as risk factors for the development of
UTIs, Dromerick and Edwards (2003) only found an increased risk of UTI to be associated with
β-Blocker use (OR & 95% CI: 4.01; 1.26-14.59) and PVR ≥ 150 mL (OR & 95% CI: 3.97; 1.249.53) among 120 stroke patients admitted to a rehabilitation service.
E10.10 Post-Void Residual Urine Testing
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Q11. Discuss the importance of the post-void residual in diagnosis of bladder
dysfunction post stroke.
Answer
1. PVR is able to determine if bladder emptying is complete.
2. PVR > 150 cc is generally regarded as abnormal.
3. Increased PVRs increases the risk of urinary tract infections.
Discussion
Borrie (1998) notes that “A true void residual (PVR) urine test is critical to determine if bladder
emptying is complete…although in/out catherization is the gold standard for determining the
PVR urine, portable bladder ultrasound is practical, noninvasive and cost-effective (Chan 1993).
A sterile culture from the catheter specimen would rule out urinary tract infection. Two
consecutive residual urines of greater than 150mL suggest a significant degree of incomplete
bladder emptying, and physical outlet obstruction should be ruled out by urology assessment
with cystoscopy. There is no consensus as to what residual urine volume is definitively
abnormal (Grosshans et al. 1993). Most would regard greater than 150 mL abnormal, but is
depends to some degree on the volume of urine voided before catheterization.”
E10.11 Diagnosis of Bladder Dysfunction
Q12. Provide a classification of bladder dysfunction post stroke.
Answers
1. Detrusor instability or hyperreflexia with urge incontinence.
2. Stress incontinence.
3. Overflow incontinence with incomplete emptying.
4. Mixed types of incontinence.
5. Functional incontinence, due to nonurinary factors.
6. Iatrogenic incontinence, due to drugs or restraints.
Discussion
Diagnosis of Various Bladder Dysfunction (from Borrie 1998)
Finding that May
Pathophysiology Confirmed
History
Residual
be Present
by Urodynamics
Urgency
Signs consistent with specific
Low
Detrusor instability
neurological disease
Stress
Demonstrated during stress
Low
(Genuine) stress incontinence
Overflowing /
Palpable bladder
High
Outlet obstruction and/or poorly
incomplete emptying Enlarged prostate
contractile detrusor
Urethral stricture
Reduced anal sphincter tone
Reduced anal sensation
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Mixed
Functional
Iatrogenic
Variable
Impaired mobility
Impaired mental state
Environmental factors
Drugs
Restraints
Variable Mixed
Low
Functional
Variable Iatrogenic
E10.12 Assessment and Management of Urinary Incontinence Post Stroke
Q13. Describe an algorithm for the assessment and management of urinary
incontinence.
Answer
1. History of symptoms to determine which type of incontinence the patient suffers from (i.e.,
urge, stress, mixed, overflow, or functional).
2. Further assessment may include a physical examination as well as urodynamic
investigations (such as a postvoid residual test or cystometry).
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Assessment and Management of Post-Stroke Urinary Incontinence
Functional / Iatrogenic Causes?
None
Restricted
Mobility
Medication
Postvoid
Residual Urine
(PVR) Test
Functional
Iatrogenic
High
(>150 ml)
Low
(<150ml)
Water
Cystometry
Overflow/
Incomplete
Emptying
Outlet
Obstructed
No
Obstruction
Relief of
Obstruction
Sterile
(or clean)
Catheterization
Leakage
Only with
Detrusor
Contractions
Leakage
without
Detrusor
Contractions
Leakage with
& without
Detrusor
Contractions
Urge
Stress
Mixed
1. Behavioural Interventions
2. Pharmacological Interventions
3. Surgical Interventions
E10.13 Treatment of Post-Stroke Urinary Dysfunction
Q14. What are the different treatment options for post-stroke urinary dysfunction?
Answers
1. Interventions used to treat UI depends on type of incontinence.
2. Initially behavioural interventions with scheduled voiding, pelvic floor exercises and
biofeedback.
3. Pharmacological interventions
4. Catheterization.
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Discussion
The intervention used to manage UI largely depends on the patient’s history and type of
incontinence. Due to the absence of strong evidence regarding treatment efficacy, Borrie
(1998) has suggested using a stepwise approach, with behavioural interventions used as first
line treatments and pharmacological and surgical interventions. This approach highlights the
fact that patients should always be treated with the least invasive intervention option.
There are few RCTs evaluating the efficacy of bladder management to treat urinary
incontinence post stroke, although the issue has been studied in other patient populations. The
choice will often be dictated by the stroke patient’s type of incontinence. In the absence of
rigorous evidence, Borrie (1998) notes that a stepwise approach is best, beginning with
behaviour intervention, progression to medication only when needed and considering surgical
interventions only as a desperate last resort.
A recent Cochrane review (Thomas et al. 2008) investigating optimal methods for prevention
and treatment of urinary incontinence after stroke in adults included the results from 12 trials
(n=724). There was a wide range of interventions including behavioural interventions (timed
voiding, pelvic floor muscles training), specialized professional input interventions (continence
nurse practitioner care), complementary therapy interventions (acupuncture, moxibustion),
pharmacotherapy (estrogen, oxybutynin, meclofenoxate) and physical therapy (sensory-motor
feedback combined with timed voiding). A pooled analysis across all interventions combined
was not performed. Two trials (Wikander 1998, Britain 2000b) offered some evidence
supporting the use of input from specialized professionals using systematic methods to help
evaluate, manage, and improve outcome of patients with continence complications. One trail
(Brittain 2000b) suggested short-term and even long-term improvements in symptoms of urinary
incontinence could be established through individualized care. While complementary
interventions appeared to be effective compared with the placebo condition, small sample sizes
and limited reporting of methodological details reduce the generalizability of the findings. While
estrogen therapy was effective in reducing the number of incontinence episodes in a week, the
therapy is generally contraindicated following stroke. There is limited evidence suggesting that
the acute stage of rehabilitation has the largest impact on urinary incontinence following stroke.
However, there is a paucity of evidence from studies done with stroke patients that helps direct
specific practice guidelines. The authors concluded that further research is required.
There are a scarcity of trials that have evaluated urinary incontinence post stroke. Brittain et al.
(1999) have highlighted the importance of distinguishing between urge incontinence and urinary
retention, since the management of each is different. A wide variety of treatments is available in
the management of incontinence following stroke. However, the pre-stroke continence status,
small sample sizes and heterogeneity of treatments and outcomes assessed limit the
generalizability of the findings. A single positive RCT was found for each of 4 differing
treatments: Moxibustion, a program of prompted voiding, biofeedback assisted pelvic floor
training and a FIM-focused rehabilitation unit.
E10.14 Behavioural Interventions for Incontinence Post Stroke
Q15. Discuss behavioural interventions for incontinence post stroke.
Answer
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1. Scheduled voiding q 2-4 hours
2. Fluid restriction.
Discussion
Dumoulin et al. (2005) conducted a systematic review investigating the benefits of behavioural
therapies used to treat urinary incontinence. The study included only four RCTs, a single cohort
study and recommendations from three clinical practice guidelines. This study found limited
evidence for the reduction of UI in male stroke patients using combination treatment including
bladder retraining with urge suppression and pelvic floor exercises. The authors concluded that
although there is increasing recognition of the benefits of using behavioral approaches as
treatment for stroke patients with a high occurrence of continual UI, the evidence remains very
limited for specific treatments used for stroke survivors with UI.
Bladder Training
Scheduled voiding programs follow a set schedule of voiding every 2-4 hours regardless of
whether the patient “needs to go” because post stroke cortical awareness of bladder fullness is
often reduced (Borrie 1998). Initiation of toileting in response to urgency, while shown to
promote continence, often does not provide enough time to void especially when mobility is
limited. Bladder training allows for lengthening of the voiding interval as the patient becomes
consistently dry (Burgio and Paurgio 1986, Borrie 1998). However, Duncan et al. (2005) suggest
that there is no evidence for or against a scheduled voiding program. These authors
recommend an individualized bladder training program and the use of prompted voiding for
incontinent stroke patients.
Scheduled Voiding programs follow a set schedule of voiding every 2-4 hours. Since cortical
awareness of bladder fullness is often reduced following a stroke, voiding is attempted
regardless of whether the patient “needs to go”. Although initiation of toileting in response to
urgency also promotes continence, it often does not provide enough time to void successfully,
particularly when mobility is limited. Thus, scheduled voiding may be useful for treating patients
with either cognitive impairment or urge incontinence. In a slight variation, bladder training also
uses a voiding schedule but differs in that the voiding interval is lengthened as the patient
becomes consistently dry.
Pelvic Floor Exercises are designed to strengthen the pelvic floor muscles through repeated
contraction and relaxation of specific muscle groups. Although these exercises were originally
developed to manage stress incontinence, rapid contractions have also been found to help
patients suppress the “urgency wave” of the relax bladder contraction (Borrie 1998).
Biofeedback is an effective but time consuming intervention that uses either audio or video
feedback to help patients identify the sensations of bladder fullness. The intension is that
patients will later recognize these bladder sensations as an early cue that they need to void.
Fluid Intake
The total measurable fluid intake should be approximately 1500 – 1800 mL per 24 hours. The
use of intravenous fluids or a feeding tube may result in fluid loads greater than 2L per day,
which will in turn compromise bladder continence (Borrie 1998).
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There is moderate evidence that prompted voiding significantly reduced the number of total
incontinent episodes. There is moderate evidence that biofeedback-assisted pelvic training and
behavioral therapy with weekly in-home visits from a nurse practitioner significantly reduces
urinary accidents and incontinence. There is moderate evidence that a functionally oriented
rehabilitation approach results in significantly less incontinence than a Bobath conventional
approach. However, treatment of urinary incontinence post stroke has not been well studied.
Further research is needed. There is moderate evidence that moxibustion can improve urinary
tract symptoms. Prompted voiding and biofeedback-assisted pelvic training plus behavioral
therapy and weekly in-home visits reduce incontinent episodes. Treatment with a functionally
oriented rehabilitation approach vs. a Bobath approach for urinary incontinence post stroke has
not been well studied.
E10.15 Pharmacological Interventions for Incontinence Post Stroke
Q16. Discuss pharmacological interventions for incontinence post stroke.
Answer
1. Pharmacologoical treatment will depend on the cause of the stroke.
2. The vast majority of bladder incontinence is due to detrusor hyperreflexia due to central loss
of inhibition.
3. Drugs with anticholinergic actions are recommended in these cases, i.e Oxybutynin.
4. For overflow incontinence due to detrusor inactivity, a cholinergic such as Bethanecol is
recommended.
5. For overflow incontinence due to outlet obstruction, an alpha-adrenergic blocker may be
recommended.
Discussion
Drug therapy should be considered an adjunct to behavioural therapy and should only be used
when behavioural interventions are either inappropriate or have had an adequate trial. The side
effects of anticholinergic medications are often underestimated, particularly in the post-stroke
population. Therefore, the goal of pharmacological therapy should be to use the lowest dose to
achieve the optimal effect with the fewest side effects (Borrie 1998).
Borrie (1998) has noted that post stroke detrusor hyperflexia treated with drugs with various
degrees of anticholinergic medications. These medications include Flavoxate, oxybutynin,
propantheline and imipramine. These drugs should be started at a low dose and increased
gradually over days, if not weeks.
Borrie (1998) has noted that Flavoxate is often worth trying initially because its direct smooth
muscle action and limited cholinergic effect leads to fewer adverse side effects. Oxybutynin is
an anticholinergic which is frequently used. Propantheline supposedly does not cross the
blood-brain barrier, with a theoretical advantage over other drugs which can lead to confusion.
Tolterodine is another anticholinergic which is said to have less influence on salivary gland
function and therefore less likely to lead to dry mouth as a complication.
- 94 -
Borrie (1998) has also noted that for patients with poor detrusor contracture, Bethanechol may
improve detrusor contracity (Sondra et al. 1979). It serves as an adjunct to intermittent
catherization. Bethanechol is discontinued if residual urines do not decrease, there is excessive
sweating, asthmatic attacks, congestive heart failure and abdominal cramps.
E10.16 Catheters for Bladder Dysfunction Post Stroke
Q17. Discuss the use of catheters for bladder dysfunction post stroke.
Answer
1. Catheters for bladder dysfunction should always be seen as a treatment of last resort.
2. Intermittent catheterization is the preferred option in urinary incontinence with overflow
incontinence.
3. An indwelling catheter should be limited to those patietne with intractable urinary retention,
continuous wetness (+/- skin breakdown) and those who have need of monitoring.
Discussion
Intermittent catheterization is the preferred management option for patients suffering from
urinary retention with overflow incontinence. The combined voided and residual volume should
not exceed 500 ml. and the frequency of catheterization should be monitored and adjusted if the
residual volume changes. Long-term in-dwelling catheters are associated with several risks,
such as chronic urinary bacteruria and bladder stones, and should only be used if intermittent
catheterization is impractical.
Gresham et al. (1995) noted that “use of indwelling catheters should be limited to patients with
incontinence due to urinary retention that cannot be otherwise treated, severely impaired
patients with skin breakdown, in whom frequent bed or clothing changes would be difficult or
painful and in patients in whom incontinence interferes with monitoring of fluid and electrolyte
balance.” Brocklehurst et al. (1985) noted that 40% of patients regain continence during the
first two weeks. The use of a catheter will inhibit that process. Again catheterization should be
reserved for exceptional circumstances (Nazarko 2003).
Bjork et al. (1984), Sabanthan et al. (1985) and Wareen et al. (1982) observed the chronic use
of indwelling catheters increases the risk of bacteria and urinary tract infection. Moreover, it has
been shown that more than three-quarters of persons catheterized for three months or more will
develop inflammatory bladder wall changes. While bacteremia can be identified by urine culture,
treatment with antibiotics should be reserved for those patients with symptomatic urinary tract
infections. Several investigators (Bennet and Diokno 1984, Maynard and Diokno 1984, Webb
1990) have noted that urinary retention can be safely managed with clean intermittent
catheterization. Intermittent catheterization can be utilized when a stroke survivor is unable to
pass urine and/or has a substantial amount of residual urine still in the bladder. To reduce the
incidence of nosocomial UTIs, the use of silver alloy-coated urinary catheters has been
recommended (Duncan et al. 2005). While the cost of these catheters is greater, they may be
more cost-effective considering the reductions in cost associated with treating bacterial UTIs.
The literature upon which this recommendation was based was not specific to stroke patients.
- 95 -
The use of indwelling catheters in stroke patients has not been well studied. There is
consensus opinion that indwelling catheters should be limited to those patients with intractable
urinary retention, skin breakdown, continuous wetness and the need for urinary monitoring. .
E10.17 Management of Bladder Retention
Q18. Describe an algorithm for the management of bladder retention?
Answer
1. Look for reversible causes of bladder retention and correct it.
2. If there is no reversible cause, need to perform urodynamic studies to determine whether it
is a sphincter problem (not opening) or a detrusor problem (hypoactive bladder).
3. If sphincter problem consider alpha-blocker medications; if not successful consider
botulinum toxin into the sphincter.
4. If detrusor problem consider cholinergic medication such as Bethanecol.
5. Once voiding begins monitor with post-void residuals.
6. If not successful catheterization is necessary; many stroke patient cannot do intermittent
catheterizations which may require an indwelling catheter.
Discussion
Management of Post-Stroke Bladder Retention
Bladder Retention
Reversible Cause?
 Immobility
 Impaction
 Obstruction
 Medication
Yes
Correct Reversible Cause
Still Retaining
Fluid
No
Intermittent Catheterization
(or, if inappropriate, In-dwelling
Catheter)
- 96 -
References
Abrams P, Cardozo L, Fall M, Griffiths D, Rosier P, Ulmsten U, van Kerrebroeck P, Victor A, Wein A. The
standardization of terminology of lower urinary tract function: Repot from the Standardization Subcommittee of the International Continence Society. Neurobiol Urodynam 2002; 21:167-178.
Barer DH. Continence after stroke: useful predictors or goal of therapy? Age Ageing
1989; 18(3):183-91.
Bean JP, Kiely DK, Cairns KD, Morris JN. Influence of poststroke urinary incontinence on disability: The
nursing home setting. Am J Phys Med Rehabil 2003; 82:175-181.
Benbow S, Sangster G, Barer D. Incontinence after stroke. Lancet 1991; 338:1602-3.
Bennett CJ, Diokno AC. Clean intermittent self catheterization in the elderly. Urology 1984; 24(1):43-45.
Bjork DT, Pelletier LL, Tight RR. Urinary tract infections with antibiotic resistant organisms
in catheterized nursing home patients. Infect Control 1984; 5(4):173-176.
Borrie M. Increased incontinence after stroke. In Teasell R (ed): Stroke Rehabilitation. Physical Medicine
and Rehabilitation: State of the Art Reviews, Hanley and Belfus, Philadelphia 1998; 12: 459-457.
Borrie MJ, Campbell AJ, Caradoc-Davies TH, Spears GF. Urinary incontinence after stroke: a
prospective study. Age Ageing 1986; 15:177-81.
Brittain KR, Peet SM, Potter JF, Castleden CM. Prevelence and management of urinary incontinence in
stroke survivors. Age Ageing 1999; 28(6):509-511.
Brittain KR, Perry SI, Peet SM, Shaw C, Dallosso H, Assassa RP, Williams K, Jagger C, Potter JF,
Castleden CM. Prevalence and impact of urinary symptoms among community-dwelling stroke survivors.
Stroke 2000; 31(4):886-91(a).
Brittain KR, Potter JF. The treatment of urinary incontinence in stroke survivors (MS9). Report for NHS
R&D Programme on Cardiovascular Disease and Stroke Project, Division of Medicine for the Elderly,
Dept of Medicine, University of Leicester, in collaboration with the MRC Incontinence Study 2000 (b).
Brocklehurst JC, Andrews K, Richards B, Laycock PJ. Incidence and correlates of incontinence in stroke
patients. J Am Geriatr Soc 1985; 33:540-542.
Brooks W. The use of practice guidelines for urinary incontinence following stroke. Bri J Nurs 2004;
13:1176-1179.
Burgio KL, Burgio LD. Behaviour therapies for urinary incontinence in the elderly. Clin Geriatr Med 1986;
2:809-27.
Burney TL, Senapati M, Desai S, Choudhary ST, Badlani GH. Acute cerebrovascular accident and lower
urinary tract dysfunction: a prospective correlation of the site of brain injury with urodynamic findings. J
Urol 1996; 156:1748-1750.
Chan H. Noninvasive bladder volume measurement. J Neurosci Nurs 1993; 25:309-12.
Doshi VS, Say JH, Young SH, Doraisamy P. Complications in stroke patients: a study carried out at the
Rehabilitation Medicine Service, Changi General Hospital. Singapore Med J 2003; 44:643-652.
Dromerick AW, Edwards DF. Relation of postvoid residual to urinary tract infection during stroke
rehabilitation. Arch Phys Med Rehabil 2003; 84:1369-1372.
- 97 -
Dumoulin C, Korner-Bitensky N, Tennenbaum C. Urinary incontinence after stroke: Identification,
assessment, and intervention by rehabilitation professionals in Canada. Stroke 2007; 38:2745-2751.
Duncan PW, Zorowitz R, Bates B, Choi JY, Glasberg JJ, Graham GD et al. Management of Adult Stroke
Rehabilitation Care: a clinical practice guideline. Stroke 2005; 36(9):e100-e143.
Fader, M. & Craggs, M. Continence problems and neurological disability. In Getliffe K & Dolman M (eds):
Promoting Continence. A Clinical Research Resource (2nd ed). Bailliere Tindall, London 2003; 337-370.
Foster and Young. The clinical and cost effectiveness of physiotherapy in the management of elderly
people following a stroke. Bradford Elderly Care and Rehabilitation Research Department, UK, 2002.
Gariballa SE. Potentially treatable causes of poor outcome in acute stroke patients with urinary
incontinence. Acta Neurol Scand 2003; 107:336-340.
Gelber DA, Good DC, Laven LJ, Verhulst SJ. Causes of urinary incontinence after acute hemispheric
stroke. Stroke 1993; 24:378-382.
Gresham GE, Duncan PW, Stason WB, Adams HP, Adelman AM, Alexander DN, Bishops DS, Diller L,
Donaldson NE, Granger CV, Holland AL, Kellyhayes M, McDowell FH, Phipps MA, Roth EJ, Siebens HC,
Tarvin GA, Trombly CA. Poststroke rehabilitation – assessment, referral and patient-management.
American Family Physician 1995; 52(2):461-470.
Grosshans C, Passadori Y, Peter B. Urinary rentention in the elderly: a study of 100
hospitalized patients. J Am Geriatr Soc 1993; 41(6):633-8.
Jawad SH, Ward AB. Study of the relationship between premorbid urinary incontinence and stroke
outcome. Clin Rehabil 1999; 13:447-452.
Jongbloed L. Prediction of function after stroke: a critical review. Stroke 1986; 17:765-776.
Jorgensen L, Engstad T, Jacobsen BK. Self-reported urinary incontinence in non-institutionalized longterm stroke survivors: A population-based study. Arch Phys Med Rehabil 2005; 86:416-420.
Kolominsky-Rabas PL, Kilz MJ, Neundoerfer B, Heuschmann PU. Impact of urinary incontinence after
stroke: results from a prospective population-based stroke register. Neurourol Urodyn 2003; 22:322-327.
Marinkovic S, Badlani G. Voiding and sexual dysfunction after cerebrovascular accidents. J Urol 2001;
165:359-370.
Maynard FM, Diokno AC. Urinary infection and complications during clean intermittent catheterization
following spinal cord injury. J Urol 1984; 132(5):943-946.
Nakayama H, Jorgensen HS, Pedersen PM, Raaschou HO, Olsen TS. Prevalence and risk factors of
incontinence after stroke. The Copenhagen Stroke Study. Stroke 1997; 28(1):58-62.
Nazarko L. Rehabilitation and continence promotion following a stroke. Nurs Times 2003; 99(4):52.
Patel M, Coshall C, Rudd AG, Wolfe CD. Natural history and effects on 2-year outcomes of urinary
incontinence after stroke. Stroke 2001; 32:122-127.
Reding MJ, Winter SW, Hochrein SA, Simon HB, Thompson MM. Urinary incontinence after unilateral
hemispheric stroke: a neurologicepidemiologic perspective. J Neuro Rehabil 1987; 1:25-30.
- 98 -
Sabanthan K, Castleden CM, Mitchell CJ. The problem of bacteriuria with indwelling urethral
catheterization. Age Ageing 1985; 14(2):85-90.
Sonda LP, Gershon C, Diokno AC, Lapides J. Further observations on the cystometric uroflowmetric
effects of bethanechol chloride on the human bladder. J Urol 1979; 122(6):775-7.
Thomas LH, Cross S, Barrett J, French B, Leathley M, Sutton CJ, Watkins C. Treatment of urinary
incontinence after stroke in adults. Cochrane Database of Systematic Reviews 2008, Issue 1. Art. No.:
CD004462. DOI: 10.1002/14651858.CD004462.pub3.
van Kuijk AA, van der Linde H, van Limbeek J. Urinary incontinence in stroke patients after admission to
a postacute inpatient rehabilitation program. Arch Phys Med Rehabil 2001; 82(10):1407-11.
Warren JW, Tenney JH, Hoopes JM, Muncie HL, Anthony WC. A prospective microbiologic study of
bacteriuria in patients with chronic indwelling urethral catheters. J Infect Dis 1982; 164(6):719-723.
Webb RJ, Lawson AL, Neal DE. Clean intermittent self-catheterization in 172 adults. Br J Urol 1990;
65(1):20-23.
Wikander B, Ekelund P., Milson, I. An evaluation of mulidisciplinary intervention governed by functional
independence measure (FIM) in incontinent stroke patients. Scand J Rehab Med 1998; 30:15-21.
- 99 -
References
Abrams P, Cardozo L, Fall M, Griffiths D, Rosier P, Ulmsten U, van Kerrebroeck P, Victor A,
Wein A. The standardization of terminology of lower urinary tract function: Repot from the
Standardization Sub-committee of the International Continence Society. Neurobiol Urodynam
2002; 21:167-178.
Adams HP, Jr., Adams RJ, Brott T, et al. Guidelines for the early management of patients with
ischemic stroke: A scientific statement from the Stroke Council of the American Stroke
Association. Stroke 2003; 34:1056-1083.
Agnew DS, Shetter AG, Segall HD, Flom RA. Thalamic pain. In Bonica J, Lindblom U, Iggo A
(eds). Advances in Pain Research and Therapy Vol. 5, Raven Press, New York, 1983, p. 941946.
Amaragiri SV, Lees TA. Elastic compression stockings for prevention of deep vein thrombosis.
Cochrane Database Syst Rev 2000; CD001484.
Andersen G, Vestergaard K, Ingeman-Nielsen M, Jensen TS. Incidence of central poststroke
pain. Pain 1995; 61:187-193.
Andre Ca, de Freitas GRa, Fukujima MMb. Prevention of deep venous thrombosis and
pulmonary embolism following stroke: a systematic review of published articles. European
Journal of Neurology 2001; 14(1):21-32.
Arboix A, Garcia-Eroles L, Massons JB, Oliveres M, Comes E. Predictive factors of early
seizures after acute cerebrovascular disease. Stroke 1997; 28:1590-1594.
Arms R, Dines D, Tinstman T. Aspiration pneumonia. Chest 1974; 65:136-139.
Bach DB, Pouget S, Belle K, Kilfoil M, Alfieri M, McEvoy J, Jackson G. An integrated team
approach to the management of patients. J Allied Health 1989; 459-468.
Barer DH. Continence after stroke: useful predictors or goal of therapy? Age Ageing
1989; 18(3):183-91.
Barer DH. The natural history and functional consequences of dysphagia after hemispheric
stroke. J Neurol Neurosurg Psychiatry 1989; 52:236-241.
Bean JP, Kiely DK, Cairns KD, Morris JN. Influence of poststroke urinary incontinence on
disability: The nursing home setting. Am J Phys Med Rehabil 2003; 82:175-181.
Benbow S, Sangster G, Barer D. Incontinence after stroke. Lancet 1991; 338:1602-3.
Bennett CJ, Diokno AC. Clean intermittent self catheterization in the elderly. Urology 1984;
24(1):43-45.
Bennett GJ, Laird JMA. Central changes contributing to neuropathic hyperalgesia. In: Willis
WD (ed), Hyperalgesia and Allodynia, Raven Press, New York, 1992, pp. 305-310.
- 100 -
Bjork DT, Pelletier LL, Tight RR. Urinary tract infections with antibiotic resistant organisms in
catheterized nursing home patients. Infect Control 1984; 5(4):173-176.
Black SE, Norris JW, Hachinski VC. Post-stroke seizures. Stroke 1983; 14:134, abstract.
Bladin CF, Alexandrov AV, Bellavance A, et al. Seizures after stroke: a prospective multicenter
study. Arch Neurol 2000; 57:1617-1622.
Boivie J. Hyperalgesia and allodynia in patients with CNS lesions. In W.D. Willis Jr. (ed.),
Hyperalgesia and Allodynia, Raven Press, New York, 1992, pp. 363-373.
Boivie J, Leijon G, Johansson I. Cental poststroke pain - a study of the mechanisms through
analyses of the sensory abnormalities. Pain 1989;37:173-185 (a).
Borrie M. Increased incontinence after stroke. In Teasell R (ed): Stroke Rehabilitation. Physical
Medicine and Rehabilitation: State of the Art Reviews, Hanley and Belfus, Philadelphia 1998;
12: 459-457.
Borrie MJ, Campbell AJ, Caradoc-Davies TH, Spears GF. Urinary incontinence after stroke: a
prospective study. Age Ageing 1986; 15:177-81.
Bounds JV, Wiebers DO, Whisnant JP, Okazaki H. Mechanism and timing of deaths from
cerebral infarctions. Stroke 1981; 12(4):474-477.
Bowsher D, Laheuerta J. Central pain in 22 patients: clinical features, somatosensory
changes and CT scan findings. J Neurol 1985; 232:237-297.
Brittain KR, Peet SM, Potter JF, Castleden CM. Prevelence and management of urinary
incontinence in stroke survivors. Age Ageing 1999; 28(6):509-511.
Brittain KR, Perry SI, Peet SM, Shaw C, Dallosso H, Assassa RP, Williams K, Jagger C, Potter
JF, Castleden CM. Prevalence and impact of urinary symptoms among community-dwelling
stroke survivors. Stroke 2000; 31(4):886-91(a).
Brittain KR, Potter JF. The treatment of urinary incontinence in stroke survivors (MS9). Report
for NHS R&D Programme on Cardiovascular Disease and Stroke Project, Division of Medicine
for the Elderly, Dept of Medicine, University of Leicester, in collaboration with the MRC
Incontinence Study 2000 (b).
Brocklehurst JC, Andrews K, Richards B, Laycock PJ. Incidence and correlates of incontinence
in stroke patients. J Am Geriatr Soc 1985; 33:540-542.
Broderick JP, Adams HP, Jr., Barsan W, et al. Guidelines for the management of spontaneous
intracerebral hemorrhage: A statement for healthcare professionals from a special writing group
of the Stroke Council, American Heart Association. Stroke 1999; 30:905-915.
Brooks W. The use of practice guidelines for urinary incontinence following stroke. Bri J Nurs
2004; 13:1176-1179.
Brown M, Glassenberg M. Mortality factors in patients with acute stroke. JAMA 1973;
224:1493-1495.
- 101 -
Burgio KL, Burgio LD. Behaviour therapies for urinary incontinence in the elderly. Clin Geriatr
Med 1986; 2:809-27.
Burn J, Dennis M, Bamford J, Sandercock P, Wade D, Warlow C 1997. Epileptic seizures after
a first stroke: the Oxfordshire Community Stroke Project. Br Med J 315:1582–1587.
Burney TL, Senapati M, Desai S, Choudhary ST, Badlani GH. Acute cerebrovascular accident
and lower urinary tract dysfunction: a prospective correlation of the site of brain injury with
urodynamic findings. J Urol 1996; 156:1748-1750.
Camilo O, Goldstein LB. Seizures and epilepsy after ischemic stroke. Stroke 2004; 35:17691775.
Chan H. Noninvasive bladder volume measurement. J Neurosci Nurs 1993; 25:309-12.
Chicago Dietetic Association, South Shore Suburban Dietetic Association and Dietitians of
Canada. Manual of clinical dietetics. 6th ed. Chicago:American Dietetic Association.
Classen DO, Kazemi N, Zubkov AY, Wijdicks EF, Rabinstein AA. Restarting anticoagulation
therapy after warfarin-associated intracerebral hemorrhage. Arch Neurol. 2008; 65(10):1313-8.
Cordonnier C, Henon, P Derambure P, Pasquier F, Leys D. Influence of pre-existing dementia
on the risk of post-stroke epileptic seizures. J Neurol Neurosurg Psychiatry 2005; 76:16491653.
Dejerine J, Roussy G. La syndrome thalamique. Rev Neurol 1906; 14:521-532 (also see
Wilkins RH, Brody IA. The thalamic syndrome. Arch Neurol 1969; 20:55).
DePippo KL, Holas MA, Reding MJ, Mandel FS, Lesser ML. Dysphagia therapy following
stroke: A controlled trial. Neurology 1994; 44:1655-1660.
De Reuck J, Krahel N, Sieben G, Orban L, de Coster W, vander Eecken H. Epilepsy in patients
with cerebral infarcts. Journal of Neurology 1980; 224(2):1432-1459.
Detsky AS, McLaughlin JR, Baker JP, et al. What is subjective global assessment of nutritional
status? JPEN 1987; 11:8-13
Diener HC, Ringelstein EB, von Kummer R et al. Prophylaxis of thrombotic and embolic events
in acute ischemic stroke with the lowmolecular-weight heparin certoparin: results of the
PROTECT Trial. Stroke 2006; 37:139-144.
Doshi VS, Say JH, Young SH, Doraisamy P. Complications in stroke patients: a study carried
out at the Rehabilitation Medicine Service, Changi General Hospital. Singapore Med J 2003;
44:643-652.
Dromerick AW, Edwards DF. Relation of postvoid residual to urinary tract infection during
stroke rehabilitation. Arch Phys Med Rehabil 2003; 84:1369-1372.
- 102 -
Dubner R. Neuronal plasticity and pain following peripheral tissue inflammation or nerve injury.
In: Bond MR, Charlton JE, Woolf CJ (eds). Pain Research and Clinical Management, Vol. 4,
Proc. VIth World Congress on Pain, Elsevier, Amsterdam, 1991, pp.263-276.
Dumas R, Woitinas F, Kutnowski M, Nikolic I, Berberich R, Abedinpour F, Zoeckler S, Gregoire
F, Jerkovic M, Egberts JFM, Stiekema JCJ. A multicentre, double-blind, randomized study to
compare the safety and efficacy of once-daily ORG 10172 and twice-daily low-dose heparin in
preventing deep-vein thrombosis in patients with acute ischaemic stroke. Age Ageing 1994;
23:512-516.
Dumoulin C, Korner-Bitensky N, Tennenbaum C. Urinary incontinence after stroke:
Identification, assessment, and intervention by rehabilitation professionals in Canada. Stroke
2007; 38:2745-2751.
Duncan PW, Zorowitz R, Bates B, Choi JY, Glasberg JJ, Graham GD et al. Management of
Adult Stroke Rehabilitation Care: a clinical practice guideline. Stroke 2005; 36(9):e100-e143.
Eckman MH, Rosand J, Knudsen KA, Singer DE, Greenberg SM. Can patients be
anticoagulated agter intracerebral hemorrhage? A decision analysis. Stroke 2003; DOI:
10.1161/01.STR.0000078311.18928.16.
Fader, M. & Craggs, M. Continence problems and neurological disability. In Getliffe K &
Dolman M (eds): Promoting Continence. A Clinical Research Resource (2nd ed). Bailliere
Tindall, London 2003; 337-370.
Ferro JM, Pinto F. Poststroke epilepsy: epidemiology, pathophysiology and management.
Drugs Aging 2004; 21:639-653.
Fields HL, Adams JE. Pain after cortical injury relieved by electrical stimulation of the internal
capsule. Brain 1974; 97:169-178.
Finegold SM. Aspiration pneumonia. Reviews of Infectious Diseases 1991; 13(Suppl 9):S737742.
Finestone HM, Greene-Finestone LS, Wilson ES, Teasell RW. Malnutrition in stroke patients on
the rehabilitation service at followup: prevalence and predictors. Arch Phys Med Rehabil 1995;
76:310-316.
Fisher RS, van Emde Boas W, Blume W, Elger C, Genton P, Lee P, Engel J Jr.Epileptic
seizures and epilepsy: definitions proposed by the International League Against Epilepsy (ILAE)
and the International Bureau for Epilepsy (IBE). Epilepsia. 2005; 46(4):470-2.
Foster and Young. The clinical and cost effectiveness of physiotherapy in the management of
elderly people following a stroke. Bradford Elderly Care and Rehabilitation Research
Department, UK, 2002.
Frese A, Husstedt IW, Ringelstein EB, Evers S. Pharmacologic Treatment of Central PostStroke Pain. Clin J Pain 2006; 22(3):252-260.
Garcin R, Lapresle J. Incoordination cerebrelleuse du membre inferieur par lesion localiseu
dans la region intern du thalamus control-lateral. Rev Neurol (Paris) 1969; 120:5.
- 103 -
Gariballa SE. Potentially treatable causes of poor outcome in acute stroke patients with urinary
incontinence. Acta Neurol Scand 2003; 107:336-340.
Gariballa SE, Parker SG, Taub N, Castleden CM. A randomized, controlled, a single-blind trial
of nutritional supplementation after acute stroke. J Parenter Enteral Nutr 1998; 22:315-319.
Gelber DA, Good DC, Laven LJ, Verhulst SJ. Causes of urinary incontinence after acute
hemispheric stroke. Stroke 1993; 24:378-382.
Gibson RS. Principles of Nutritional Assessment. New York, Oxford University Press, 1990.
Gilad R, Sadeh M, Rapoport A, Dabby R, Boaz M, Lampl Y. Monotherapy of lamotrigine versus
carbamazepine in patients with poststroke seizure. Clin Neuropharmacol 2007; 30:189-195.
Gill P, Nahum A. Improving detection of venous thromboembolism: new technology holds
promise for early, precise diagnosis. Postgrad Med 2000; 108(4):24-40.
Giroud M, Gras P, Fayolle H, Andre N, Soichot P, Dumas R. Early seizures after acute stroke:
a study of 1,640 cases. Epilepsia 1994; 35:959-964.
Gordon A. Best practive guidelines for treatment of central pain after stroke. In: Henry JL,
Panju A, Yashpal K, eds. Central Neuropathic Pain: Focus on Poststroke Pain. Seattle: IASP
Press, 2007.
Gordon C, Hewer RL, Wade DT. Dysphagia in acute stroke. Br Med J 1987; 295:411-414.
Gottlieb D, Kipnis M, Sister E, Vardi Y, Brill S. Validation of the 50 ml3 drinking test for
evaluation of poststroke dysphagia. Disabil Rehabil 1996; 18(10):529-532.
Greenfield LJ, Michna BA. 12-year clinical-experience with the Greenfield vena-caval filter.
Surgery 1988; 104(4):706-712.
Gresham GE, Duncan PW, Stason WB, Adams HP, Adelman AM, Alexander DN, Bishops DS,
Diller L, Donaldson NE, Granger CV, Holland AL, Kellyhayes M, McDowell FH, Phipps MA, Roth
EJ, Siebens HC, Tarvin GA, Trombly CA. Poststroke rehabilitation – assessment, referral and
patient-management. American Family Physician 1995; 52(2):461-470.
Grosshans C, Passadori Y, Peter B. Urinary rentention in the elderly: a study of 100
hospitalized patients. J Am Geriatr Soc 1993; 41(6):633-8.
Guigoz Y, Vellas B, Garry P. The Mini Nutritional Assessment: A practical assessment tool for
grading the nutritional state of elderly patients. Facts Res Gerontol 1994; 4:15-59.
Gupta SR, Naheedy MH, Elias D. Post infarction seizures: A clinical study. Stroke 1988;
19:1477-81.
Hanning C, WuttgeHanning A, Hormann M, Hermann I. A cinematographic study of the
pathologic mechanism of aspiration pneumonia. Fortschv Rontgenstr 1989; 159(3):260-267.
- 104 -
Hansson P. Post-stroke pain case study: Clinical characteristics, therapeutic options and longterm follow-up. Eur J Neurol 2004; 11(Suppl 1):22-30.
Heart and Stroke Foundation of Ontario. Improving Recognition and Management of Dysphagia
in Acute Stroke. 2002.
Hillbom M, Erila T, Sotaniemi K, Tatlisumak T, Sarna S, Kaste M. Enoxaparin vs heparin for
prevention of deep-vein thrombosis in acute ischaemic stroke: a randomized, double-blind
study. Acta Neurol Scand 2002;106(2):84-92.
Holas MA, DePippo KL, Reding MJ. Aspiration and relative risk of medical complications
following stroke. Arch Neurol 1994; 51:1051-1053.
Holmes GL. The electroencephalogram as a predictor of seizures following cerebral infarction.
Clinical Electroencephalography 1980; 11(2):83-86.
Horner J, Massey EW. Silent aspiration following stroke. Neurology 1988; 38:317-319(a).
Horner J, Massey EW, Riski JE, Lathrop DL, Chase KN. Aspiration following stroke: Clinical
correlates and outcome. Neurology 1988;38:1359-1362(b).
Huxley EJ, Viroslav J, Gray WR, Pierce AK. Pharyngeal aspiration in normal adults and
patients with depressed consciousness. Am J Med 1978; 64:564-568.
Imberti D, Prisco D. Venous thromboembolism prophylaxis in medical patients: future
perspectives. Thromb Res 2005; 116(5):365-375.
Jawad SH, Ward AB. Study of the relationship between premorbid urinary incontinence and
stroke outcome. Clin Rehabil 1999; 13:447-452.
Jensen TS, Lenz FA. Central post-stroke pain: a challenge for the scientist and the clinician.
Pain 1995; 61:161-164.
Johnson ER, McKenzie SW, Sievers A. Aspiration pneumonia in stroke. Arch Phys Med
Rehabil 1993; 74:973-976.
Jongbloed L. Prediction of function after stroke: a critical review. Stroke 1986; 17:765-776.
Jorgensen L, Engstad T, Jacobsen BK. Self-reported urinary incontinence in noninstitutionalized long-term stroke survivors: A population-based study. Arch Phys Med Rehabil
2005; 86:416-420.
Kay R, Wong KS, Yu YL et al. Low-molecular weight heparin for the treatment of acute
ischemic stroke. N Engl J Med 1995; 333:1588-1593.
Kidd D, Lawson J, Nesbitt R, MacMahon J. The natural history and clinical consequences of
aspiration in acute stroke. Quarterly J Med 1995; 88:409-413.
Kilpatrick CJ, Davis SM, Tress BM. Epileptic seizures in acute stroke. Arch Neurol 1990;
47:157-60.
- 105 -
Kolominsky-Rabas PL, Kilz MJ, Neundoerfer B, Heuschmann PU. Impact of urinary
incontinence after stroke: results from a prospective population-based stroke register.
Neurourol Urodyn 2003; 22:322-327.
Kotila M, Waltimo O. Epilepsy after stroke. Epilepsia 1992; 33:495-498.
Labovitz DL, Hauser WA, Sacco RL. Prevalence and predictors of early seizures and status
epilexticus after first stroke. Neurology 2001; 57:200-206.
Lampl C, Yazdi K, Roper C. Amitriptyline in the prophylazis of central poststroke pain.
Preliminary results of 39 patients in a placebo-controlled, long-term study. Stroke 2002;
33:3030-2.
Lancman ME, Golimstock A, Norscimi J, Granillo R. Risk factors for developing seizures after
stroke. Epilepsia 1993; 34:141-143.
Langmore SE, Terpenning MS, Schork A, Chen Y, Murray JT, Lopatin D, Loesche WJ.
Predictors of aspiration pneumonia: how important is dysphagia? Dysphagia 1998; 13(2):69-81.
Leijon G, Boivie J, Johansson I. Central poststroke pain - neurological symptoms and pain
characteristics. Pain 1989; 36:13-25(a).
Leijon G, Boivie J. Central post-stroke pain – a controlled trail of amitriptyline and
carbamazepine. Pain 1989; 36:27-36.
Linden P, Siebens AA. Dysphagia: predicting laryngeal penetration. Arch Phys Med Rehabil
1983; 64:281-284.
Logemann JA. Evaluation and treatment of swallowing disorders. San Diego, CA: CollegeHill
Press, 1983.
Loh L, Nathan PW, Schott GD. Pain due to lesions of central nervous system removed by
sympathetic block. Br Med J 1981; 282:1026-1028.
Louis S, McDowell F. Epileptic seizures in nonembolic cerebral infarction. Archives of
Neurology 1967; 17(4):414.
Marinkovic S, Badlani G. Voiding and sexual dysfunction after cerebrovascular accidents. J
Urol 2001; 165:359-370.
Martino R, Pron G, Diamant N. Screening for oropharyngeal dysphagia in stroke: insufficient
evidence for guidelines. Dysphagia 2000; 15:19-30.
Maynard FM, Diokno AC. Urinary infection and complications during clean intermittent
catheterization following spinal cord injury. J Urol 1984; 132(5):943-946.
Mazzone C, Chiodo Grandi F, Sandercock PAG, Miccio M, Salvi R. Physical methods for
preventing deep vein thrombosis in stroke. Coochrane Database of Systematic Reviews 2004
Issue 4. Art. No.: CD001922. DOI: 10.1002/14651858.CD001922.pub2.
- 106 -
McCarthy ST, Turner J. Low-dose subcutaneous heparin in the prevention of deep-vein
thrombosis and pulmonary emboli following acute stroke. Age Aging 1986; 15:84-88.
McCarthy ST, Turner JJ, Robertson D, Hawkey CJ, Macey DJ. Low-dose heparin as a
prophylaxis against deep-vein thrombosis after acute stroke. Lancet 1977; 11:800-801.
McQuay HJ, Carroll D, Glynn CJ. Dose-response for analgesic effect of amitriptyline in chronic
pain. Anaeathesia 1993; 106:3-8.
Meyer JS, Charney JZ, Rivera VM, Mathew NT. Cerebral embolization: prospective clinical
analysis of 42 cases. Stroke 1971; 2:541-554.
Milazzo LS, Bouchard J, Lund DA. The swallowing process: effects of aging and stroke.
Physical Medicine and Rehabilitation: State of the Art Reviews 1989; 3(3):489-499.
Mucke L, Maciewicz R. Clinical management of neuropathic pain. Neurol Clin 1987; 5(4):649662.
Muir KW, Watt A, Baxter G, Grosset DG, Lees KR. Randomized trial of graded compression
stockings for prevention of deep-vein thrombosis after acute stroke. QJM 2000; 93(6):359-64.
Muller-Lissner SA, Fimmel CJ, Will N, et al. Effect of gastric and transpyloric tubes on gastric
emptying and duodenogastric reflux. Gastroenterology 1982; 83:1276-1279.
Nakayama H, Jorgensen HS, Pedersen PM, Raaschou HO, Olsen TS. Prevalence and risk
factors of incontinence after stroke. The Copenhagen Stroke Study. Stroke 1997; 28(1):58-62.
Nazarko L. Rehabilitation and continence promotion following a stroke. Nurs Times 2003;
99(4):52.
Olsen TS, Hogenhave H, Thage O. Epilepsy after stroke. Neurology 1987; 37:1209-11.
Pagni CA. Central pain due to spinal cord and brainstem damage. In Wall PD, Melzack R
(eds). Textbook of Pain, Churchill Livingstone, London, 1984, p. 481-495.
Paolucci S, Silverstri G, Lubich S, Pratesi L, Traballesi M, Gigli GL. Post stroke late seizures
and their role in rehabilitation of inpatients. Epilepsia 1997; 38(3):266-270.
Patel M, Coshall C, Rudd AG, Wolfe CD. Natural history and effects on 2-year outcomes of
urinary incontinence after stroke. Stroke 2001; 32:122-127.
PIOPED Investigators. Value of the ventilation/perfusion scan in acute pulmonary embolism:
results of the prospective investigation of pulmonary embolism diagnosis (PIOPED). JAMA
1990; 263(20):2753-2759.
Platt J. Dysphagia Management for Long Term Care: A Manual for Nurses and Other
Healthcare Professionals. Clinical and Educational Services, Hamilton, Ont, 2001.
Prasad BK, Banerjee AK, Howard H. Incidence of deep vein thrombosis and the effect of
pneumatic compression of the calf in elderly hemiplegics. Age Aging 1982; 11:42-44.
- 107 -
Prins MH, Gelsema R, Sing AK, Van Heerde LR, den Ottolander GJH. Prophylaxis of deep
venous thrombosis with a low-molecularweight heparin (Kabi 2165/Fragmin) in stroke patients.
Haemostasis 1989;19:245-250.
Ramsey DJ, Smithard DG, Kalra L. Early assessments of dysphagia and aspiration risk in
acute stroke patients. Stroke 2003; 34(5):1252-1257.
Reding MJ, Winter SW, Hochrein SA, Simon HB, Thompson MM. Urinary incontinence after
unilateral hemispheric stroke: a neurologicepidemiologic perspective. J Neuro Rehabil 1987;
1:25-30.
Reith J, Jorgensen HS, Nakayama H, Raaschou HO, Olsen TS. Seizures in acute stroke:
predictors and prognostic significance. The Copenhagen Stroke Study. Stroke 1997; 28:15851589.
Sabanthan K, Castleden CM, Mitchell CJ. The problem of bacteriuria with indwelling urethral
catheterization. Age Ageing 1985; 14(2):85-90.
Sandset PM, Dahl T, Stiris M, et al. A double-blind and randomized placebo-controlled trial of
low-molecular-weight heparin once daily to prevent deep-vein thrombosis in acute ischemic
stroke. Seminars in Thrombosis and Hemostasis 1990; 16:25-33.
Scmidt EV, Smirnov VE, Ryabova VS. Results of the sevenyear prospective study of stroke
patients. Stroke 1988; 19(8):942-949.
Schmidt J, Holas M, Halvorson K, Reding M. Videofluroscopic evidence of aspiration predict
pneumonia and death but not dehydration following stroke. Dysphagia 1994; 9:711.
Sellars C, Bowie L, Bagg J, et al. Risk factors for chest infection in acute stroke: a prospective
cohort study. Stroke 2007; 38:2284-2291
Sharma JC, Fletcher S, Vassallo M, Ross I. What influences outcome of strokepyrexia or
dysphagia? Int J Clin Pract 2001; 55(1):1720.
Sherman DG, Albers GW, Bladin C et al. The efficacy and safety of enoxaparin versus
unfractionated heparin for the prevention of venous thromboembolism after acute ischaemic
stroke (PREVAIL Study): an openlabel randomised comparison. Lancet 2007; 369:1347-1355.
Shinton RA, Gill JS, Melnick SC. The frequency, characteristics and prognosis of epileptic
seizures at the onset of stroke. J Neurol Neurosurg Psychiatry 1988; 51:273-76.
Silver F, Norris J, Lewis A, Hachinski V. Early mortality following stroke: a retrospective review.
Stroke 1984; 15(3):492-496.
Sioson ER, Crowe WE, Dawson NV. Occult proximal deep vein thrombosis: Its prevalence
among patients admitted to a rehabilitation hospital. Arch Phys Med Rehabil 1988; 69:183-185.
Smithard DG, O'Neill PA, Park C, Morris J, Wyatt R, England R, Martin DF. Complications and
outcome after acute stroke. Does dysphagia matter? Stroke 1996; 27:1200-1204.
- 108 -
Sonda LP, Gershon C, Diokno AC, Lapides J. Further observations on the cystometric
uroflowmetric effects of bethanechol chloride on the human bladder. J Urol 1979; 122(6):775-7.
Splaingard ML, Hutchins B, Sulton LD, Chaudhuri G. Aspiration in rehabilitation patients:
videofluoroscopy vs bedside clinical assessment. Arch Phys Med Rehab 1988; 69:637-640.
Steele CM. Emergency room assessment and intervention for dysphagia: a pilot project. J
Speech Language Pathology and Audiology 2002; 26:100-110
Sundaram MBM, Chow F. Seizures associated with spontaneous subarachnoid hemorrhage.
Can J Neurol Sci 1986; 13:229-31.
Sung CY, Chu NS. Epileptic seizures in intracerebral hemorrhage. J Neurol Neurosurg
Psychiatry 1986; 52:1273-76.
Tasker RR. Pain resulting from central nervous system pathology (central pain). In Bonica JJ
(ed). The Management of Pain, Lea & Febiger, Malvern, PA, Vol 1, 2nd ed, 1990, p 264-283.
Teasell RW, Bach D, McRae M. Prevalence and recovery of aspiration poststroke: a
retrospective analysis. Dysphagia 1994; 9(1):35-39.
Teasell RW, Foley NC, Salter K, Bhogal SK, Jutai J, Speechley MR. Evidence-Based Review
of Stroke Rehabilitation (11th edition). Canadian Stroke Network; 2008.
Teasell RW, Marchuk Y, McRae M, Finestone HM. Pneumonia associated with aspiration
following stroke. Arch Phys Med Rehabil 1996; 77:707-709.
Terre R, Mearin F. Oropharyngeal dysphagia after the acute phase of stroke: predictors of
aspiration. Neurogastroenterol Motil 2006; 18(3):200-205.
Thomas LH, Cross S, Barrett J, French B, Leathley M, Sutton CJ, Watkins C. Treatment of
urinary incontinence after stroke in adults. Cochrane Database of Systematic Reviews 2008,
Issue 1. Art. No.: CD004462. DOI: 10.1002/14651858.CD004462.pub3.
Tobin MJ. Aspiration pneumonia. In: Dantzker DR (ed). Cardiopulmonary Critical Care. New
York, Grune and Stratton, 1986.
Turpie AG, Gent M, Cote R, Levine MN, Ginsberg JS, Powers PJ, Leclerc J, Geerts W, Jay R,
Neemeh J. A low-molecular-weight heparinoid compared with unfractionated heparin in the
prevention of deep vein thrombosis in patients with acute ischemic stroke. Ann Intern Med
1992; 117(5):353-357.
Turpie AGG, Levine MN, Hirsh J, Carter CJ, Jay RM, Andrew M, Magnani HN, Hull RD, Gent M.
Double-blind randomised trial of ORG 10172 low-molecular-weight heparinoid in prevention of
deep-vein thrombosis in thrombotic stroke. Lancet 1987; 1:523-526.
Usefulness of a low molecular weight heparinoid in improving outcomes at 7 days and 3 months
after stroke – results of the trial of Org 10172 in acute stroke treatment (TOAST). Stroke 1998;
29:286-286.
- 109 -
van Kuijk AA, van der Linde H, van Limbeek J. Urinary incontinence in stroke patients after
admission to a postacute inpatient rehabilitation program. Arch Phys Med Rehabil 2001;
82(10):1407-11.
Veis S, Logemann J. Swallowing disorders in persons with cerebrovascular accidents. Arch
Phys Med Rehabil 1985; 66:373-374.
Vernino S, Brown RD, Jr., Sejvar JJ, Sicks JD, Petty GW, O'Fallon WM. Cause-specific
mortality after first cerebral infarction: a population-based study. Stroke 2003; 34(8):1828-1832.
Vespa PM, O'Phelan K, Shah M et al. Acute seizures after intracerebral hemorrhage: a factor in
progressive midline shift and outcome. Neurology. 2003; 60:1441-1446.
Vestergaard K, Nielsen J, Andersen G, Ingeman-Nielsen M, Arendt-Nielsen L, Jensen TS.
Sensory abnormalities in consecutive, unselected patients with central post-stroke pain. Pain
1995; 61:177-185.
Wall PD. Neuropathic pain and injured nerve: central mechanisms. Br Med Bull 1991; 47:631643.
Warren JW, Tenney JH, Hoopes JM, Muncie HL, Anthony WC. A prospective microbiologic
study of bacteriuria in patients with chronic indwelling urethral catheters. J Infect Dis 1982;
164(6):719-723.
Wasay M, Khan S, Zaki KS, Khealani BA, Kamal A, Azam I, Khatri IA. A non-randomized study
of safety and efficacy of heparin for DVT prophylaxis in intracerebral haemorrhage. J Pak Med
Assoc. 2008; 58(7):362-364.
Webb RJ, Lawson AL, Neal DE. Clean intermittent self-catheterization in 172 adults. Br J Urol
1990; 65(1):20-23.
Wiebe S, Butler JT 1998. Poststroke seizures and epilepsy. In: Teasell R (editor): Physical
Medicine and Rehabilitation: State of the Art Reviews. Philadelphia: Hanley and Belfus. pp.
405–422.
Wiebe-Velazquez S, Blume WT. Seizures. In: Teasell RW (ed). Physical Medicine and
Rehabilitation: State of the Art Reviews. Long-Term Consequences of Stroke. Philadelphia,
Hanley & Belfus, 1993; 7(1):73-87.
Wikander B, Ekelund P., Milson, I. An evaluation of mulidisciplinary intervention governed by
functional independence measure (FIM) in incontinent stroke patients. Scand J Rehab Med
1998; 30:15-21.
- 110 -